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Alb-cre+/MYC+
Product ID:
C001339
Strain:
C57BL/6JCya
Status:
Description:
The MYC oncogene family comprises regulatory genes and proto-oncogenes that encode transcription factors, involved in various cellular processes such as the cell cycle, apoptosis, DNA repair, and metabolism. Members include c-Myc (MYC), l-Myc (MYCL), and n-Myc (MYCN). c-Myc (MYC) is a basic helix-loop-helix leucine zipper (bHLHZip) transcription factor, which forms heterodimers with Max protein to bind DNA and regulate the expression of approximately 15% of genes, thereby participating in key cellular processes such as cell proliferation, apoptosis, DNA repair, and metabolism. In many cancers, c-Myc is overexpressed, leading to uncontrolled cell proliferation and tumor growth, such as in Burkitt's lymphoma where c-Myc gene rearrangement is common. Dysregulation of the MYC oncogene plays a crucial role in tumorigenesis, predominantly through transcriptional dysregulation resulting in overexpression of c-Myc protein.
Alb-Cre+/MYC+ mice are generated by crossing H11-CAG-LSL-hMYC-IRES-EGFP mice (Catalog Number: C001338), which conditionally express the human c-Myc oncogene, with Alb-Cre mice that express Cre recombinase specifically in hepatocytes under the control of the Alb promoter. The Cre-mediated recombination results in the deletion of the transcriptional stop sequence (Loxp-Stop-Loxp, LSL) in H11-CAG-LSL-hMYC-IRES-EGFP mice, leading to overexpression of the MYC oncogene in the liver and subsequent carcinogenesis. This model, therefore, spontaneously develops liver cancer with an early onset.
The MYC oncogene family comprises regulatory genes and proto-oncogenes that encode transcription factors, involved in various cellular processes such as the cell cycle, apoptosis, DNA repair, and metabolism. Members include c-Myc (MYC), l-Myc (MYCL), and n-Myc (MYCN). c-Myc (MYC) is a basic helix-loop-helix leucine zipper (bHLHZip) transcription factor, which forms heterodimers with Max protein to bind DNA and regulate the expression of approximately 15% of genes, thereby participating in key cellular processes such as cell proliferation, apoptosis, DNA repair, and metabolism. In many cancers, c-Myc is overexpressed, leading to uncontrolled cell proliferation and tumor growth, such as in Burkitt's lymphoma where c-Myc gene rearrangement is common. Dysregulation of the MYC oncogene plays a crucial role in tumorigenesis, predominantly through transcriptional dysregulation resulting in overexpression of c-Myc protein.
Alb-Cre+/MYC+ mice are generated by crossing H11-CAG-LSL-hMYC-IRES-EGFP mice (Catalog Number: C001338), which conditionally express the human c-Myc oncogene, with Alb-Cre mice that express Cre recombinase specifically in hepatocytes under the control of the Alb promoter. The Cre-mediated recombination results in the deletion of the transcriptional stop sequence (Loxp-Stop-Loxp, LSL) in H11-CAG-LSL-hMYC-IRES-EGFP mice, leading to overexpression of the MYC oncogene in the liver and subsequent carcinogenesis. This model, therefore, spontaneously develops liver cancer with an early onset.
B6-hALB/hTFRC
Product ID:
C001730
Strain:
C57BL/6NCya
Status:
Description:
The ALB gene encodes albumin, mainly produced in the liver, and is the most abundant protein in human plasma, accounting for 60% to 65% of total plasma protein. The proprotein encoded by ALB is processed to produce a functional protein, and the EPI-X4 peptide derived from this protein is an endogenous inhibitor of the CXCR4 chemokine receptor. Albumin plays a role in regulating plasma colloid osmotic pressure, helping to maintain blood circulation and isolating and transporting many metabolites within the body, especially insoluble hydrophobic metabolites [1]. Human Serum Albumin (HSA) is an important carrier protein involved in the transport of a variety of endogenous molecules, including hormones, fatty acids, and metabolic products, as well as exogenous drugs. As a natural carrier protein, HSA has multiple ligand binding sites and a plasma half-life of up to 19 days, making it a promising drug carrier. Several HSA-based drug delivery systems have been approved for clinical trials [2-3]. In addition, albumin is also the main transporter of zinc, calcium, and magnesium in plasma, binding approximately 80% of all plasma zinc and approximately 45% of circulating calcium and magnesium, with an affinity ranking of zinc > calcium > magnesium [4]. Diseases associated with the ALB gene include hyperthyroxinemia, familial serum albumin abnormality, and analbuminemia [5].
The Transferrin receptor (TFRC) gene encodes Transferrin Receptor 1 (TFR1), a protein that is expressed at low levels in most normal cells but shows increased expression in highly proliferative cells, such as basal epidermal cells, intestinal epithelium, and certain activated immune cells. Brain capillary endothelial cells, which constitute the blood-brain barrier (BBB), also express this receptor at high levels [6]. TFR1 plays a critical role in maintaining iron metabolism and homeostasis by facilitating receptor-mediated endocytosis of iron-bound transferrin (Tf) via Tf cycling, thereby promoting iron uptake [7]. Cellular iron deficiency can lead to apoptosis, while cellular transformation requires substantial iron to sustain proliferation, with iron overload contributing to tumor progression. The high expression of TFR1 in many tumors makes it a potential tumor marker, offering a target for therapies to inhibit tumor growth and metastasis [6]. Moreover, TFR1 is implicated in anemia and iron metabolism disorders. Studies have shown that elevated TFR1 expression in cardiomyocytes is associated with exacerbated inflammation in myocarditis patients [8].
B6-hALB/hTFRC mice are a dual gene humanized model of Alb and Tfrc, obtained by crossing B6-hALB (HSA) mice (Catalog number: C001492) with B6-hTFRC (CDS) mice (Catalog number: C001584). This model can be used for the development of ALB/TFRC-targeted therapeutic drugs, as well as for the research on drug development using human serum albumin (HSA) as a carrier or drug delivery across the blood-brain barrier (BBB), and for in vivo pharmacodynamic and pharmacokinetic studies.
The ALB gene encodes albumin, mainly produced in the liver, and is the most abundant protein in human plasma, accounting for 60% to 65% of total plasma protein. The proprotein encoded by ALB is processed to produce a functional protein, and the EPI-X4 peptide derived from this protein is an endogenous inhibitor of the CXCR4 chemokine receptor. Albumin plays a role in regulating plasma colloid osmotic pressure, helping to maintain blood circulation and isolating and transporting many metabolites within the body, especially insoluble hydrophobic metabolites [1]. Human Serum Albumin (HSA) is an important carrier protein involved in the transport of a variety of endogenous molecules, including hormones, fatty acids, and metabolic products, as well as exogenous drugs. As a natural carrier protein, HSA has multiple ligand binding sites and a plasma half-life of up to 19 days, making it a promising drug carrier. Several HSA-based drug delivery systems have been approved for clinical trials [2-3]. In addition, albumin is also the main transporter of zinc, calcium, and magnesium in plasma, binding approximately 80% of all plasma zinc and approximately 45% of circulating calcium and magnesium, with an affinity ranking of zinc > calcium > magnesium [4]. Diseases associated with the ALB gene include hyperthyroxinemia, familial serum albumin abnormality, and analbuminemia [5].
The Transferrin receptor (TFRC) gene encodes Transferrin Receptor 1 (TFR1), a protein that is expressed at low levels in most normal cells but shows increased expression in highly proliferative cells, such as basal epidermal cells, intestinal epithelium, and certain activated immune cells. Brain capillary endothelial cells, which constitute the blood-brain barrier (BBB), also express this receptor at high levels [6]. TFR1 plays a critical role in maintaining iron metabolism and homeostasis by facilitating receptor-mediated endocytosis of iron-bound transferrin (Tf) via Tf cycling, thereby promoting iron uptake [7]. Cellular iron deficiency can lead to apoptosis, while cellular transformation requires substantial iron to sustain proliferation, with iron overload contributing to tumor progression. The high expression of TFR1 in many tumors makes it a potential tumor marker, offering a target for therapies to inhibit tumor growth and metastasis [6]. Moreover, TFR1 is implicated in anemia and iron metabolism disorders. Studies have shown that elevated TFR1 expression in cardiomyocytes is associated with exacerbated inflammation in myocarditis patients [8].
B6-hALB/hTFRC mice are a dual gene humanized model of Alb and Tfrc, obtained by crossing B6-hALB (HSA) mice (Catalog number: C001492) with B6-hTFRC (CDS) mice (Catalog number: C001584). This model can be used for the development of ALB/TFRC-targeted therapeutic drugs, as well as for the research on drug development using human serum albumin (HSA) as a carrier or drug delivery across the blood-brain barrier (BBB), and for in vivo pharmacodynamic and pharmacokinetic studies.
B6-hCALCA
Product ID:
C001523
Strain:
C57BL/6JCya
Status:
Description:
Calcitonin-related polypeptide alpha (CALCA) is a protein-encoded gene, also known as CALC1, CGRP, or CGRP-α. Multiple genetic factors and epigenetic modifications regulate CALCA gene expression, and it forms peptide hormones calcitonin (CT), α-isoform of calcitonin gene-related peptide (CGRP), and katacalcin through tissue-specific RNA alternative splicing and non-active precursor protein cleavage in transcription and translation. Calcitonin is synthesized and secreted by thyroid parafollicular cells, mainly involved in regulating calcium levels and phosphorus metabolism in bones and kidneys. It can reduce the concentration of calcium and phosphorus in the plasma and inhibit the absorption of calcium and phosphorus. CGRP mainly acts as a vasodilator and antimicrobial peptide, which can cause dilatation of coronary arteries, cerebral vessels, and systemic vessels, and help to regulate blood pressure. CGRP is also widely distributed in the pain pathways of the peripheral and central nervous system (CNS) of the human body, and its receptors are also expressed in the pain pathways. CGRP participates in the transmission of pain signals from the periphery to the CNS and plays a key role in pain regulation, which is related to the pathogenesis of a variety of pain diseases and related syndromes, including somatic pain, visceral pain, neuropathic pain, inflammatory pain, and migraine. Katacalcin mainly exists as a peptide that can effectively lower plasma calcium, and its effect of lowering serum calcium levels is almost the same as that of calcitonin. CALCA gene polymorphism is associated with a variety of diseases, including reflex sympathetic dystrophy syndrome, complex regional pain syndrome, ischemic stroke, Parkinson's disease, ovarian cancer, bone mineral density, migraine, schizophrenia, bipolar disorder, and primary hypertension [1-5]. CALCA is a potential target for new therapies for a variety of diseases. Currently, various CALCA antagonists are being developed for the treatment of migraine and primary hypertension, and research on targeting CALCA for diseases such as Alzheimer's disease and Parkinson's disease is also ongoing [6-7].
This strain is a humanized mouse model of the Calca gene. Using gene editing technology, the base sequence of the mouse Calca gene from the start codon to the 3’UTR region was replaced by the corresponding sequence in the human CALCA gene, while the 5’UTR region of the mouse Calca gene was retained. Homozygous B6-hCALCA mice are viable and fertile and can be used to study the mechanisms of various physiological and pathological processes such as blood pressure regulation, cell proliferation, cell apoptosis, vascular biology, physiological bone marrow production, inflammation, tumor growth, and research on CALCA-targeted migraine drugs and therapies.
Calcitonin-related polypeptide alpha (CALCA) is a protein-encoded gene, also known as CALC1, CGRP, or CGRP-α. Multiple genetic factors and epigenetic modifications regulate CALCA gene expression, and it forms peptide hormones calcitonin (CT), α-isoform of calcitonin gene-related peptide (CGRP), and katacalcin through tissue-specific RNA alternative splicing and non-active precursor protein cleavage in transcription and translation. Calcitonin is synthesized and secreted by thyroid parafollicular cells, mainly involved in regulating calcium levels and phosphorus metabolism in bones and kidneys. It can reduce the concentration of calcium and phosphorus in the plasma and inhibit the absorption of calcium and phosphorus. CGRP mainly acts as a vasodilator and antimicrobial peptide, which can cause dilatation of coronary arteries, cerebral vessels, and systemic vessels, and help to regulate blood pressure. CGRP is also widely distributed in the pain pathways of the peripheral and central nervous system (CNS) of the human body, and its receptors are also expressed in the pain pathways. CGRP participates in the transmission of pain signals from the periphery to the CNS and plays a key role in pain regulation, which is related to the pathogenesis of a variety of pain diseases and related syndromes, including somatic pain, visceral pain, neuropathic pain, inflammatory pain, and migraine. Katacalcin mainly exists as a peptide that can effectively lower plasma calcium, and its effect of lowering serum calcium levels is almost the same as that of calcitonin. CALCA gene polymorphism is associated with a variety of diseases, including reflex sympathetic dystrophy syndrome, complex regional pain syndrome, ischemic stroke, Parkinson's disease, ovarian cancer, bone mineral density, migraine, schizophrenia, bipolar disorder, and primary hypertension [1-5]. CALCA is a potential target for new therapies for a variety of diseases. Currently, various CALCA antagonists are being developed for the treatment of migraine and primary hypertension, and research on targeting CALCA for diseases such as Alzheimer's disease and Parkinson's disease is also ongoing [6-7].
This strain is a humanized mouse model of the Calca gene. Using gene editing technology, the base sequence of the mouse Calca gene from the start codon to the 3’UTR region was replaced by the corresponding sequence in the human CALCA gene, while the 5’UTR region of the mouse Calca gene was retained. Homozygous B6-hCALCA mice are viable and fertile and can be used to study the mechanisms of various physiological and pathological processes such as blood pressure regulation, cell proliferation, cell apoptosis, vascular biology, physiological bone marrow production, inflammation, tumor growth, and research on CALCA-targeted migraine drugs and therapies.
B6-hCALCRL
Product ID:
C001497
Strain:
C57BL/6JCya
Status:
Description:
Calcitonin receptor-like receptor (CALCRL) is a seven-transmembrane G protein-coupled receptor encoded by the CALCRL gene. It mediates the pleiotropic effects of calcitonin gene-related peptide (CGRP) and adrenal medullary peptide (ADM), two structurally related neuropeptides that are potent vasodilators and play an important role in blood pressure regulation [1]. In addition, CALCRL is involved in various other biological processes, including cell proliferation, cell death regulation, vascular biology, and inflammation [2]. CALCRL is currently being investigated as a new target for the treatment of migraine [3]. In solid tumors, antibodies that target CALCRL have been shown to reduce tumor growth by either disrupting angiogenesis or by directly inhibiting cancer cell proliferation [4]. CALCRL is also expressed in normal CD34+ hematopoietic progenitor cells, and CGRP and ADM can directly stimulate these cells to form colonies in vitro, suggesting a role for CALCRL in physiological bone marrow generation [5].
This strain represents a humanized mouse model of the Calcrl gene. Using gene editing technology, the sequence encoding the extracellular domain of the mouse Calcrl gene was replaced with the corresponding sequence from the human CALCRL gene. This model can be used to study the mechanisms of various physiological and pathological processes, such as blood pressure regulation, cell proliferation, cell death, vascular biology, physiological bone marrow generation, inflammation, and tumor growth, as well as the development of CALCRL-targeted migraine drugs and therapies. Homozygous B6-hCALCRL mice are viable and fertile.
Calcitonin receptor-like receptor (CALCRL) is a seven-transmembrane G protein-coupled receptor encoded by the CALCRL gene. It mediates the pleiotropic effects of calcitonin gene-related peptide (CGRP) and adrenal medullary peptide (ADM), two structurally related neuropeptides that are potent vasodilators and play an important role in blood pressure regulation [1]. In addition, CALCRL is involved in various other biological processes, including cell proliferation, cell death regulation, vascular biology, and inflammation [2]. CALCRL is currently being investigated as a new target for the treatment of migraine [3]. In solid tumors, antibodies that target CALCRL have been shown to reduce tumor growth by either disrupting angiogenesis or by directly inhibiting cancer cell proliferation [4]. CALCRL is also expressed in normal CD34+ hematopoietic progenitor cells, and CGRP and ADM can directly stimulate these cells to form colonies in vitro, suggesting a role for CALCRL in physiological bone marrow generation [5].
This strain represents a humanized mouse model of the Calcrl gene. Using gene editing technology, the sequence encoding the extracellular domain of the mouse Calcrl gene was replaced with the corresponding sequence from the human CALCRL gene. This model can be used to study the mechanisms of various physiological and pathological processes, such as blood pressure regulation, cell proliferation, cell death, vascular biology, physiological bone marrow generation, inflammation, and tumor growth, as well as the development of CALCRL-targeted migraine drugs and therapies. Homozygous B6-hCALCRL mice are viable and fertile.
B6-hB2M&HLA-A2.1/mB2m KO
Product ID:
C001696
Strain:
C57BL/6N;6JCya
Status:
Description:
The B2M gene encodes beta-2 microglobulin, a serum protein on the surface of nearly all nucleated cells along with the major histocompatibility complex (MHC) class I heavy chain. It is an essential component for transporting MHC class I proteins to the cell surface. Human leukocyte antigen (HLA), or the major histocompatibility complex (MHC), is a group of protein molecules on the surface of antigen-presenting cells responsible for antigen presentation. HLA mainly includes HLA class I, HLA class II, and HLA class III. HLA class I molecules (such as HLA-A, HLA-B, and HLA-C) primarily present antigens to CD8+ T cells and play a central role in the immune system. Through antigen presentation by HLA class I, the body can effectively recognize abnormal peptides, triggering targeted immune responses for immune clearance. Studies have shown that peptide vaccines composed of covalently linked minimal cytotoxic T lymphocyte (CTL) and T helper cell (TH) epitopes have significant effects in inducing cellular immune responses [1]. Due to species differences between mice and humans, and the varying ability of different HLA molecule subtypes to present different antigens, mouse-derived HLA cannot effectively simulate the immune response of human HLA subtypes. Therefore, constructing mice carrying human HLA genes helps to advance the study of HLA-restricted cytotoxic responses, such as identifying immunodominant HLA-restricted CTL epitopes and optimizing DNA vaccine constructs for human use [2-3].
HLA-A2.1 is a subtype of class I HLA and is one of the most common HLA subtypes worldwide. HLA-A2.1 plays an important role in the immune system, especially in the presentation of antigens such as viruses, bacteria, and parasites to cytotoxic T cells (CD8+ T cells). This presentation process is essential for the immune response of the human body to a variety of pathogens, particularly in the response to human immunodeficiency virus (HIV), hepatitis B virus (HBV), and hepatitis C virus (HCV). In addition, HLA-A2.1 is also involved in the immune response to cancer cells, further emphasizing its importance in the human immune system.
The B6-hB2M&HLA-A2.1/mB2m KO mice are a humanized model obtained by mating H11-hB2M&HLA-A2.1 mice (Catalog Number: I001138) with B2m gene knockout mouse model (Catalog Number: S-KO-19919). While knocking out the mouse B2m gene, the chimeric H2-K1 HLA-A2.1 gene is integrated into the H11 safe harbor locus, which may be able to recapitulate the immune response of the human HLA-A*0201 (MHCI) subtype. This model can play an important role in studying the determinants of HLA-A2.1-restricted cytotoxic T lymphocytes (CTLs) and the development of potential viral vaccines and helps research the human immune response to a variety of antigens.
The B2M gene encodes beta-2 microglobulin, a serum protein on the surface of nearly all nucleated cells along with the major histocompatibility complex (MHC) class I heavy chain. It is an essential component for transporting MHC class I proteins to the cell surface. Human leukocyte antigen (HLA), or the major histocompatibility complex (MHC), is a group of protein molecules on the surface of antigen-presenting cells responsible for antigen presentation. HLA mainly includes HLA class I, HLA class II, and HLA class III. HLA class I molecules (such as HLA-A, HLA-B, and HLA-C) primarily present antigens to CD8+ T cells and play a central role in the immune system. Through antigen presentation by HLA class I, the body can effectively recognize abnormal peptides, triggering targeted immune responses for immune clearance. Studies have shown that peptide vaccines composed of covalently linked minimal cytotoxic T lymphocyte (CTL) and T helper cell (TH) epitopes have significant effects in inducing cellular immune responses [1]. Due to species differences between mice and humans, and the varying ability of different HLA molecule subtypes to present different antigens, mouse-derived HLA cannot effectively simulate the immune response of human HLA subtypes. Therefore, constructing mice carrying human HLA genes helps to advance the study of HLA-restricted cytotoxic responses, such as identifying immunodominant HLA-restricted CTL epitopes and optimizing DNA vaccine constructs for human use [2-3].
HLA-A2.1 is a subtype of class I HLA and is one of the most common HLA subtypes worldwide. HLA-A2.1 plays an important role in the immune system, especially in the presentation of antigens such as viruses, bacteria, and parasites to cytotoxic T cells (CD8+ T cells). This presentation process is essential for the immune response of the human body to a variety of pathogens, particularly in the response to human immunodeficiency virus (HIV), hepatitis B virus (HBV), and hepatitis C virus (HCV). In addition, HLA-A2.1 is also involved in the immune response to cancer cells, further emphasizing its importance in the human immune system.
The B6-hB2M&HLA-A2.1/mB2m KO mice are a humanized model obtained by mating H11-hB2M&HLA-A2.1 mice (Catalog Number: I001138) with B2m gene knockout mouse model (Catalog Number: S-KO-19919). While knocking out the mouse B2m gene, the chimeric H2-K1 HLA-A2.1 gene is integrated into the H11 safe harbor locus, which may be able to recapitulate the immune response of the human HLA-A*0201 (MHCI) subtype. This model can play an important role in studying the determinants of HLA-A2.1-restricted cytotoxic T lymphocytes (CTLs) and the development of potential viral vaccines and helps research the human immune response to a variety of antigens.
B6-hSEZ6
Product ID:
C001916
Strain:
C57BL/6NCya
Status:
Description:
The Sez6 gene primarily encodes a Seizure-related homolog protein 6 (SEZ6), a cell-surface type I transmembrane glycoprotein that is an N-glycosylated protein containing five short consensus repeat (SCR)/sushi domains and two or three CUB domains in its extracellular domain [1]. Gene expression is highly restricted in normal adult tissues, found almost exclusively in the central nervous system (CNS), particularly in neurons (e.g., in the cerebral cortex, hippocampus), with low expression in the testis and some gastrointestinal tissues. SEZ6 is involved in neuronal development and function, notably in regulating dendrite elongation and branching, synaptic plasticity, and may also function as a complement regulator by inhibiting C3 convertases, in addition to being a novel trafficking protein of the kainate receptor (KAR) [2]. Associated diseases include neurodevelopmental and psychiatric disorders such as epilepsy (especially febrile seizures), schizophrenia, and Alzheimer's disease. Furthermore, SEZ6 overexpression has been detected in various high-grade neuroendocrine malignancies (e.g., small cell lung cancer (SCLC), medullary thyroid carcinomas), making it a novel therapeutic target in cancer [1].
The B6-hSEZ6 mouse is a humanized model constructed by gene-editing technology, in which the p.20 to partial intron 3 of mouse Sez6 is replaced with Human-Mouse chimeric CDS (Human SEZ6 Extracellular + Mouse Sez6 Intracellular)-3'UTR of Mouse Sez6-WPRE-BGH pA cassette. The murine signal peptide is remained. This model can be used for the research of the pathological mechanisms of neurodevelopmental and psychiatric disorders such as epilepsy (especially febrile seizures), schizophrenia, and Alzheimer's disease, and some cancers, as well as the development of relevant treatment methods, and the screening, development, and pre-clinical evaluation of SEZ6-targeted drugs.
The Sez6 gene primarily encodes a Seizure-related homolog protein 6 (SEZ6), a cell-surface type I transmembrane glycoprotein that is an N-glycosylated protein containing five short consensus repeat (SCR)/sushi domains and two or three CUB domains in its extracellular domain [1]. Gene expression is highly restricted in normal adult tissues, found almost exclusively in the central nervous system (CNS), particularly in neurons (e.g., in the cerebral cortex, hippocampus), with low expression in the testis and some gastrointestinal tissues. SEZ6 is involved in neuronal development and function, notably in regulating dendrite elongation and branching, synaptic plasticity, and may also function as a complement regulator by inhibiting C3 convertases, in addition to being a novel trafficking protein of the kainate receptor (KAR) [2]. Associated diseases include neurodevelopmental and psychiatric disorders such as epilepsy (especially febrile seizures), schizophrenia, and Alzheimer's disease. Furthermore, SEZ6 overexpression has been detected in various high-grade neuroendocrine malignancies (e.g., small cell lung cancer (SCLC), medullary thyroid carcinomas), making it a novel therapeutic target in cancer [1].
The B6-hSEZ6 mouse is a humanized model constructed by gene-editing technology, in which the p.20 to partial intron 3 of mouse Sez6 is replaced with Human-Mouse chimeric CDS (Human SEZ6 Extracellular + Mouse Sez6 Intracellular)-3'UTR of Mouse Sez6-WPRE-BGH pA cassette. The murine signal peptide is remained. This model can be used for the research of the pathological mechanisms of neurodevelopmental and psychiatric disorders such as epilepsy (especially febrile seizures), schizophrenia, and Alzheimer's disease, and some cancers, as well as the development of relevant treatment methods, and the screening, development, and pre-clinical evaluation of SEZ6-targeted drugs.
B6-hAGT/hREN/huPCSK9
Product ID:
C001922
Strain:
C57BL/6Cya
Status:
Description:
The B6-hAGT/hREN/huPCSK9 mouse is a humanized model obtained by mating the hREN x hAGT mouse (catalog No.: C001336) with the B6-huPCSK9 mouse (catalog No.: C001617). This model can be used for mechanism research on chronic hypertension, various metabolic diseases, neurodegenerative diseases, and tumorigenesis, as well as the development of relevant treatment methods.
The B6-hAGT/hREN/huPCSK9 mouse is a humanized model obtained by mating the hREN x hAGT mouse (catalog No.: C001336) with the B6-huPCSK9 mouse (catalog No.: C001617). This model can be used for mechanism research on chronic hypertension, various metabolic diseases, neurodegenerative diseases, and tumorigenesis, as well as the development of relevant treatment methods.
B6-hDPP4 (line1)
Product ID:
I001187
Strain:
C57BL/6NCya
Status:
Description:
The DPP4 gene (CD26) encodes dipeptidyl peptidase 4, an intrinsic type II transmembrane glycoprotein and a serine exopeptidase involved in glucose and insulin metabolism and immune regulation. The DPP4 protein is a functional receptor for the Middle East Respiratory Syndrome Coronavirus (MERS-CoV). The spike protein of MERS-CoV binds to DPP4, mediating the virus's attachment to host cells and promoting virus-cell fusion, thereby initiating infection [1-2]. Studies have found that the DPP4 protein may interact with the S1 domain of the spike glycoprotein of COVID-19, aiding in enhancing the transmission efficiency of viral particles [3]. Experimental evidence has shown that hDPP4 transgenic mice infected with MERS-CoV experience high mortality and severe pneumonia [4]. These mice infected with Manis javanica HKU4-related coronavirus (MjHKU4r-CoV-1) develop mild to moderate pulmonary histological damage [5]. Thus, gene-edited mice expressing human DPP4 protein are important tools for studying coronavirus infections. Additionally, DPP4 expression is severely dysregulated in diseases such as inflammation, cancer, obesity, and diabetes. DPP4 is highly expressed in the intestine, where it selectively cleaves N-terminal dipeptides from various substrates, including incretins, to inactivate multiple bioactive peptides. Since incretins like glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) are crucial for regulating postprandial insulin secretion, inhibiting DPP4 to elevate endogenous GLP-1 and GIP levels to increase insulin levels has become an important treatment method for type 2 diabetes (T2D) [6].
The B6-hDPP4(line 1) mouse is a humanized model constructed by gene editing technology to replace a partial region of the mouse Dpp4 gene with the human DPP4 gene CDS sequence. This model can be used to study the infection mechanisms of viruses such as MERS-CoV and COVID-19, as well as to develop related virus vaccines. Additionally, this model can be utilized to develop DPP4 inhibitor therapies. Additionally, Cyagen Biosciences has developed B6-hDPP4(line 2) mice (Catalog ID: I001188) on the C57BL/6JCya background strain and BALB/c-hDPP4(line 2) mice (Catalog ID: I001189) on the BALB/cAnCya background strain. These two models replace the mouse Dpp4 gene p.S29 to part of intron 2 with the "Human DPP4 CDS-rBG pA" expression cassette, meeting the experimental needs for different strain backgrounds.
The DPP4 gene (CD26) encodes dipeptidyl peptidase 4, an intrinsic type II transmembrane glycoprotein and a serine exopeptidase involved in glucose and insulin metabolism and immune regulation. The DPP4 protein is a functional receptor for the Middle East Respiratory Syndrome Coronavirus (MERS-CoV). The spike protein of MERS-CoV binds to DPP4, mediating the virus's attachment to host cells and promoting virus-cell fusion, thereby initiating infection [1-2]. Studies have found that the DPP4 protein may interact with the S1 domain of the spike glycoprotein of COVID-19, aiding in enhancing the transmission efficiency of viral particles [3]. Experimental evidence has shown that hDPP4 transgenic mice infected with MERS-CoV experience high mortality and severe pneumonia [4]. These mice infected with Manis javanica HKU4-related coronavirus (MjHKU4r-CoV-1) develop mild to moderate pulmonary histological damage [5]. Thus, gene-edited mice expressing human DPP4 protein are important tools for studying coronavirus infections. Additionally, DPP4 expression is severely dysregulated in diseases such as inflammation, cancer, obesity, and diabetes. DPP4 is highly expressed in the intestine, where it selectively cleaves N-terminal dipeptides from various substrates, including incretins, to inactivate multiple bioactive peptides. Since incretins like glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) are crucial for regulating postprandial insulin secretion, inhibiting DPP4 to elevate endogenous GLP-1 and GIP levels to increase insulin levels has become an important treatment method for type 2 diabetes (T2D) [6].
The B6-hDPP4(line 1) mouse is a humanized model constructed by gene editing technology to replace a partial region of the mouse Dpp4 gene with the human DPP4 gene CDS sequence. This model can be used to study the infection mechanisms of viruses such as MERS-CoV and COVID-19, as well as to develop related virus vaccines. Additionally, this model can be utilized to develop DPP4 inhibitor therapies. Additionally, Cyagen Biosciences has developed B6-hDPP4(line 2) mice (Catalog ID: I001188) on the C57BL/6JCya background strain and BALB/c-hDPP4(line 2) mice (Catalog ID: I001189) on the BALB/cAnCya background strain. These two models replace the mouse Dpp4 gene p.S29 to part of intron 2 with the "Human DPP4 CDS-rBG pA" expression cassette, meeting the experimental needs for different strain backgrounds.
B6-hDPP4 (line 2)
Product ID:
I001188
Strain:
C57BL/6JCya
Status:
Description:
The DPP4 gene (CD26) encodes dipeptidyl peptidase 4, an intrinsic type II transmembrane glycoprotein and a serine exopeptidase involved in glucose and insulin metabolism and immune regulation. The DPP4 protein is a functional receptor for the Middle East Respiratory Syndrome Coronavirus (MERS-CoV). The spike protein of MERS-CoV binds to DPP4, mediating the virus's attachment to host cells and promoting virus-cell fusion, thereby initiating infection [1-2]. Studies have found that the DPP4 protein may interact with the S1 domain of the spike glycoprotein of COVID-19, aiding in enhancing the transmission efficiency of viral particles [3]. Experimental evidence has shown that hDPP4 transgenic mice infected with MERS-CoV experience high mortality and severe pneumonia [4]. These mice infected with Manis javanica HKU4-related coronavirus (MjHKU4r-CoV-1) develop mild to moderate pulmonary histological damage [5]. Thus, gene-edited mice expressing human DPP4 protein are important tools for studying coronavirus infections. Additionally, DPP4 expression is severely dysregulated in diseases such as inflammation, cancer, obesity, and diabetes. DPP4 is highly expressed in the intestine, where it selectively cleaves N-terminal dipeptides from various substrates, including incretins, to inactivate multiple bioactive peptides. Since incretins like glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) are crucial for regulating postprandial insulin secretion, inhibiting DPP4 to elevate endogenous GLP-1 and GIP levels to increase insulin levels has become an important treatment method for type 2 diabetes (T2D) [6].
The B6-hDPP4(line 2) mouse is a humanized model constructed by gene editing technology to replace a partial region of the mouse Dpp4 gene with the human DPP4 gene CDS sequence. This model can be used to study the infection mechanisms of viruses such as MERS-CoV and COVID-19, as well as to develop related virus vaccines. Additionally, this model can be utilized to develop DPP4 inhibitor therapies. Similar models include the B6-hDPP4(line 1) mouse (Catalog ID: I001187), constructed on the C57BL/6NCya background strain, which replaces the sequence of the mouse Dpp4 gene with the human DPP4 gene CDS sequence, and the BALB/c-hDPP4(line 2) mouse (Catalog ID: I001189), constructed on the BALB/cAnCya background strain. These models meet the experimental needs of different strain backgrounds.
The DPP4 gene (CD26) encodes dipeptidyl peptidase 4, an intrinsic type II transmembrane glycoprotein and a serine exopeptidase involved in glucose and insulin metabolism and immune regulation. The DPP4 protein is a functional receptor for the Middle East Respiratory Syndrome Coronavirus (MERS-CoV). The spike protein of MERS-CoV binds to DPP4, mediating the virus's attachment to host cells and promoting virus-cell fusion, thereby initiating infection [1-2]. Studies have found that the DPP4 protein may interact with the S1 domain of the spike glycoprotein of COVID-19, aiding in enhancing the transmission efficiency of viral particles [3]. Experimental evidence has shown that hDPP4 transgenic mice infected with MERS-CoV experience high mortality and severe pneumonia [4]. These mice infected with Manis javanica HKU4-related coronavirus (MjHKU4r-CoV-1) develop mild to moderate pulmonary histological damage [5]. Thus, gene-edited mice expressing human DPP4 protein are important tools for studying coronavirus infections. Additionally, DPP4 expression is severely dysregulated in diseases such as inflammation, cancer, obesity, and diabetes. DPP4 is highly expressed in the intestine, where it selectively cleaves N-terminal dipeptides from various substrates, including incretins, to inactivate multiple bioactive peptides. Since incretins like glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) are crucial for regulating postprandial insulin secretion, inhibiting DPP4 to elevate endogenous GLP-1 and GIP levels to increase insulin levels has become an important treatment method for type 2 diabetes (T2D) [6].
The B6-hDPP4(line 2) mouse is a humanized model constructed by gene editing technology to replace a partial region of the mouse Dpp4 gene with the human DPP4 gene CDS sequence. This model can be used to study the infection mechanisms of viruses such as MERS-CoV and COVID-19, as well as to develop related virus vaccines. Additionally, this model can be utilized to develop DPP4 inhibitor therapies. Similar models include the B6-hDPP4(line 1) mouse (Catalog ID: I001187), constructed on the C57BL/6NCya background strain, which replaces the sequence of the mouse Dpp4 gene with the human DPP4 gene CDS sequence, and the BALB/c-hDPP4(line 2) mouse (Catalog ID: I001189), constructed on the BALB/cAnCya background strain. These models meet the experimental needs of different strain backgrounds.
BALB/c-hDPP4 (line 2)
Product ID:
I001189
Strain:
BALB/cAnCya
Status:
Description:
The DPP4 gene (CD26) encodes dipeptidyl peptidase 4, an intrinsic type II transmembrane glycoprotein and a serine exopeptidase involved in glucose and insulin metabolism and immune regulation. The DPP4 protein is a functional receptor for the Middle East Respiratory Syndrome Coronavirus (MERS-CoV). The spike protein of MERS-CoV binds to DPP4, mediating the virus's attachment to host cells and promoting virus-cell fusion, thereby initiating infection [1-2]. Studies have found that the DPP4 protein may interact with the S1 domain of the spike glycoprotein of COVID-19, aiding in enhancing the transmission efficiency of viral particles [3]. Experimental evidence has shown that hDPP4 transgenic mice infected with MERS-CoV experience high mortality and severe pneumonia [4]. These mice infected with Manis javanica HKU4-related coronavirus (MjHKU4r-CoV-1) develop mild to moderate pulmonary histological damage [5]. Thus, gene-edited mice expressing human DPP4 protein are important tools for studying coronavirus infections. Additionally, DPP4 expression is severely dysregulated in diseases such as inflammation, cancer, obesity, and diabetes. DPP4 is highly expressed in the intestine, where it selectively cleaves N-terminal dipeptides from various substrates, including incretins, to inactivate multiple bioactive peptides. Since incretins like glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) are crucial for regulating postprandial insulin secretion, inhibiting DPP4 to elevate endogenous GLP-1 and GIP levels to increase insulin levels has become an important treatment method for type 2 diabetes (T2D) [6].
The BALB/c-hDPP4(line 2) mouse is a humanized model constructed by gene editing technology to replace a partial region of the mouse Dpp4 gene with the human DPP4 gene CDS sequence. This model can be used to study the infection mechanisms of viruses such as MERS-CoV and COVID-19, as well as to develop related virus vaccines. Additionally, this model can be utilized to develop DPP4 inhibitor therapies. Similar models include the B6-hDPP4(line 1) mouse (Catalog ID: I001187), constructed on the C57BL/6NCya background strain, which replaces the sequence of the mouse Dpp4 gene with the human DPP4 gene CDS sequence, and the B6-hDPP4(line 2) mouse (Catalog ID: I001188), constructed on the C57BL/6JCya background strain. These models meet the experimental needs of different strain backgrounds.
The DPP4 gene (CD26) encodes dipeptidyl peptidase 4, an intrinsic type II transmembrane glycoprotein and a serine exopeptidase involved in glucose and insulin metabolism and immune regulation. The DPP4 protein is a functional receptor for the Middle East Respiratory Syndrome Coronavirus (MERS-CoV). The spike protein of MERS-CoV binds to DPP4, mediating the virus's attachment to host cells and promoting virus-cell fusion, thereby initiating infection [1-2]. Studies have found that the DPP4 protein may interact with the S1 domain of the spike glycoprotein of COVID-19, aiding in enhancing the transmission efficiency of viral particles [3]. Experimental evidence has shown that hDPP4 transgenic mice infected with MERS-CoV experience high mortality and severe pneumonia [4]. These mice infected with Manis javanica HKU4-related coronavirus (MjHKU4r-CoV-1) develop mild to moderate pulmonary histological damage [5]. Thus, gene-edited mice expressing human DPP4 protein are important tools for studying coronavirus infections. Additionally, DPP4 expression is severely dysregulated in diseases such as inflammation, cancer, obesity, and diabetes. DPP4 is highly expressed in the intestine, where it selectively cleaves N-terminal dipeptides from various substrates, including incretins, to inactivate multiple bioactive peptides. Since incretins like glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) are crucial for regulating postprandial insulin secretion, inhibiting DPP4 to elevate endogenous GLP-1 and GIP levels to increase insulin levels has become an important treatment method for type 2 diabetes (T2D) [6].
The BALB/c-hDPP4(line 2) mouse is a humanized model constructed by gene editing technology to replace a partial region of the mouse Dpp4 gene with the human DPP4 gene CDS sequence. This model can be used to study the infection mechanisms of viruses such as MERS-CoV and COVID-19, as well as to develop related virus vaccines. Additionally, this model can be utilized to develop DPP4 inhibitor therapies. Similar models include the B6-hDPP4(line 1) mouse (Catalog ID: I001187), constructed on the C57BL/6NCya background strain, which replaces the sequence of the mouse Dpp4 gene with the human DPP4 gene CDS sequence, and the B6-hDPP4(line 2) mouse (Catalog ID: I001188), constructed on the C57BL/6JCya background strain. These models meet the experimental needs of different strain backgrounds.
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