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huTP53
Product ID:
C001640
Strain:
C57BL/6JCya
Status:
Description:
The TRP53 (TP53 in humans) gene is a critical tumor suppressor gene that encodes the p53 protein, often called the "guardian of the genome." This protein is expressed at low levels in normal cells but becomes highly activated in response to various cellular stresses like DNA damage, hypoxia, and oncogene activation [1]. The p53 protein is a transcription factor that regulates a vast network of target genes, directing the cell's response to stress by inducing cell cycle arrest, DNA repair, apoptosis (programmed cell death), or senescence (permanent growth arrest). Its activity is crucial for maintaining genomic stability and preventing malignant transformation [2]. Mutations in TP53 are the most frequent genetic alterations in human cancers, found in over 50% of all malignancies. These mutations not only cause a loss of the protein's tumor-suppressing function but can also confer new, "gain-of-function" oncogenic properties that promote tumor growth, invasion, and metastasis. While most commonly associated with a wide range of cancers, including hereditary cancers like Li-Fraumeni syndrome, abnormal p53 activity has also been linked to non-neoplastic conditions such as certain developmental and neurodegenerative disorders, like Alzheimer's and Huntington's disease, and bone marrow failure syndrome. The p53 protein is expressed ubiquitously across most cellular tissues due to its fundamental role in cellular homeostasis [3].
huTP53 mouse is a humanized model constructed via gene editing technology, in which the region from ATG start codon to downstream of 3'UTR of mouse Trp53 is replaced with the region from ATG start codon to downstream of 3'UTR of human TP53. Initial research has shown that breeding the homozygous line results in a very small number of pups. While heterozygous females can breed normally, their maternal instincts are poor, with instances of cannibalism and occasional deaths of pups due to a failure to thrive. huTP53 mouse can be used for mechanistic research on a wide range of cancers, including hereditary cancers like Li-Fraumeni syndrome and preclinical studies of TP53-targeted drugs.
The TRP53 (TP53 in humans) gene is a critical tumor suppressor gene that encodes the p53 protein, often called the "guardian of the genome." This protein is expressed at low levels in normal cells but becomes highly activated in response to various cellular stresses like DNA damage, hypoxia, and oncogene activation [1]. The p53 protein is a transcription factor that regulates a vast network of target genes, directing the cell's response to stress by inducing cell cycle arrest, DNA repair, apoptosis (programmed cell death), or senescence (permanent growth arrest). Its activity is crucial for maintaining genomic stability and preventing malignant transformation [2]. Mutations in TP53 are the most frequent genetic alterations in human cancers, found in over 50% of all malignancies. These mutations not only cause a loss of the protein's tumor-suppressing function but can also confer new, "gain-of-function" oncogenic properties that promote tumor growth, invasion, and metastasis. While most commonly associated with a wide range of cancers, including hereditary cancers like Li-Fraumeni syndrome, abnormal p53 activity has also been linked to non-neoplastic conditions such as certain developmental and neurodegenerative disorders, like Alzheimer's and Huntington's disease, and bone marrow failure syndrome. The p53 protein is expressed ubiquitously across most cellular tissues due to its fundamental role in cellular homeostasis [3].
huTP53 mouse is a humanized model constructed via gene editing technology, in which the region from ATG start codon to downstream of 3'UTR of mouse Trp53 is replaced with the region from ATG start codon to downstream of 3'UTR of human TP53. Initial research has shown that breeding the homozygous line results in a very small number of pups. While heterozygous females can breed normally, their maternal instincts are poor, with instances of cannibalism and occasional deaths of pups due to a failure to thrive. huTP53 mouse can be used for mechanistic research on a wide range of cancers, including hereditary cancers like Li-Fraumeni syndrome and preclinical studies of TP53-targeted drugs.
Trp53-KO
Product ID:
C001203
Strain:
C57BL/6JCya
Status:
Description:
The tumor protein p53 (TP53) gene encodes P53 oncoprotein, a tumor suppressor protein containing transcriptional activation, DNA binding, and oligomerization domains. The P53 oncoprotein responds to diverse cellular stresses to regulate the expression of target genes, thereby inducing cell cycle arrest, apoptosis, senescence, DNA repair, or changes in metabolism. Mutations in this gene are associated with a variety of human cancers, including hereditary cancers such as Li-Fraumeni syndrome.
This strain is a mouse model lacking Trp53, which is a gene homologous to human TP53. Homozygous Trp53-KO male mice develop normally but are prone to spontaneous tumors. Homozygous Trp53-KO mice developed tumors, mainly lymphomas, and sarcomas, at three to six months of age, and heterozygous mice developed tumors at about 10 months of age. Homozygous males are viable and fertile, but homozygous females have reduced survival at weaning.
This strain is a mouse model lacking Trp53, which is a gene homologous to human TP53. Homozygous Trp53-KO male mice develop normally but are prone to spontaneous tumors. Homozygous Trp53-KO mice developed tumors, mainly lymphomas, and sarcomas, at three to six months of age, and heterozygous mice developed tumors at about 10 months of age. Homozygous males are viable and fertile, but homozygous females have reduced survival at weaning.
The tumor protein p53 (TP53) gene encodes P53 oncoprotein, a tumor suppressor protein containing transcriptional activation, DNA binding, and oligomerization domains. The P53 oncoprotein responds to diverse cellular stresses to regulate the expression of target genes, thereby inducing cell cycle arrest, apoptosis, senescence, DNA repair, or changes in metabolism. Mutations in this gene are associated with a variety of human cancers, including hereditary cancers such as Li-Fraumeni syndrome.
This strain is a mouse model lacking Trp53, which is a gene homologous to human TP53. Homozygous Trp53-KO male mice develop normally but are prone to spontaneous tumors. Homozygous Trp53-KO mice developed tumors, mainly lymphomas, and sarcomas, at three to six months of age, and heterozygous mice developed tumors at about 10 months of age. Homozygous males are viable and fertile, but homozygous females have reduced survival at weaning.
This strain is a mouse model lacking Trp53, which is a gene homologous to human TP53. Homozygous Trp53-KO male mice develop normally but are prone to spontaneous tumors. Homozygous Trp53-KO mice developed tumors, mainly lymphomas, and sarcomas, at three to six months of age, and heterozygous mice developed tumors at about 10 months of age. Homozygous males are viable and fertile, but homozygous females have reduced survival at weaning.
Trp53&Apc dKO
Product ID:
C001909
Strain:
C57BL/6JCya
Status:
Description:
The tumor protein p53 (TP53) gene encodes P53 oncoprotein, a tumor suppressor protein containing transcriptional activation, DNA binding, and oligomerization domains. The P53 oncoprotein responds to diverse cellular stresses to regulate the expression of target genes, thereby inducing cell cycle arrest, apoptosis, senescence, DNA repair, or changes in metabolism.
The adenomatous polyposis coli (APC) gene is a tumor suppressor gene, the protein it encodes plays a key regulatory role in the Wnt/β-catenin signaling pathway [1]. The APC protein can antagonize the Wnt signaling pathway, assisting in regulating cell migration, adhesion, transcriptional activation, and apoptosis. More than 10% of human tumors have mutations in the APC gene, and most colorectal cancers have mutations in the APC gene [2]. Defects in the APC gene lead to the occurrence of familial adenomatous polyposis (FAP), characterized by hundreds to thousands of adenomatous polyps in the rectum. This is an autosomal dominant precancerous disease, which usually develops into malignant tumors [1-2]. Disease-related mutations in the APC gene are highly prevalent in a small region known as the mutation cluster region (MCR), which usually leads to the production of truncated proteins [3-4]. In mice, either Apc gene deletion or multiple intestinal neoplasia (Min) mutations that result in the production of truncated APC proteins cause phenotypes similar to human familial adenomatous polyposis (FAP) and/or colorectal tumors [5-9].
Trp53 & Apc dKO mice are a double-gene knockout model obtained by mating Trp53 KO mice (catalog number: C001203) with Apc KO mice (catalog number: C001511). Homozygous knockout of the Apc gene is lethal. Trp53 & Apc dKO mice can be used for the study of the mechanisms of tumors or tumor-related diseases such as familial adenomatous polyposis (FAP) and colorectal cancer.
The tumor protein p53 (TP53) gene encodes P53 oncoprotein, a tumor suppressor protein containing transcriptional activation, DNA binding, and oligomerization domains. The P53 oncoprotein responds to diverse cellular stresses to regulate the expression of target genes, thereby inducing cell cycle arrest, apoptosis, senescence, DNA repair, or changes in metabolism.
The adenomatous polyposis coli (APC) gene is a tumor suppressor gene, the protein it encodes plays a key regulatory role in the Wnt/β-catenin signaling pathway [1]. The APC protein can antagonize the Wnt signaling pathway, assisting in regulating cell migration, adhesion, transcriptional activation, and apoptosis. More than 10% of human tumors have mutations in the APC gene, and most colorectal cancers have mutations in the APC gene [2]. Defects in the APC gene lead to the occurrence of familial adenomatous polyposis (FAP), characterized by hundreds to thousands of adenomatous polyps in the rectum. This is an autosomal dominant precancerous disease, which usually develops into malignant tumors [1-2]. Disease-related mutations in the APC gene are highly prevalent in a small region known as the mutation cluster region (MCR), which usually leads to the production of truncated proteins [3-4]. In mice, either Apc gene deletion or multiple intestinal neoplasia (Min) mutations that result in the production of truncated APC proteins cause phenotypes similar to human familial adenomatous polyposis (FAP) and/or colorectal tumors [5-9].
Trp53 & Apc dKO mice are a double-gene knockout model obtained by mating Trp53 KO mice (catalog number: C001203) with Apc KO mice (catalog number: C001511). Homozygous knockout of the Apc gene is lethal. Trp53 & Apc dKO mice can be used for the study of the mechanisms of tumors or tumor-related diseases such as familial adenomatous polyposis (FAP) and colorectal cancer.
Trp53-KO
Product ID:
S-KO-05567
Strain:
C57BL/6JCya
Status:
Description:
Trp53 is located on chromosome 11 of mice. Nuclease Technology was used to design sgRNA; Trp53 knockout mice were obtained by applying high-throughput electroporation of fertilized eggs. After sexual maturity, sperm were collected for cryopreservation.
Trp53 is located on chromosome 11 of mice. Nuclease Technology was used to design sgRNA; Trp53 knockout mice were obtained by applying high-throughput electroporation of fertilized eggs. After sexual maturity, sperm were collected for cryopreservation.
Trp53-KO
Product ID:
S-KO-05566
Strain:
C57BL/6JCya
Status:
Description:
Trp53 is located on chromosome 11 of mice. Nuclease Technology was used to design sgRNA; Trp53 knockout mice were obtained by applying high-throughput electroporation of fertilized eggs. After sexual maturity, sperm were collected for cryopreservation.
Trp53 is located on chromosome 11 of mice. Nuclease Technology was used to design sgRNA; Trp53 knockout mice were obtained by applying high-throughput electroporation of fertilized eggs. After sexual maturity, sperm were collected for cryopreservation.
Trp53-KO
Product ID:
S-KO-16097
Strain:
C57BL/6NCya
Status:
Description:
Trp53 is located on chromosome 11 of mice. Nuclease Technology was used to design sgRNA; Trp53 knockout mice were obtained by applying high-throughput electroporation of fertilized eggs. After sexual maturity, sperm were collected for cryopreservation.
Trp53 is located on chromosome 11 of mice. Nuclease Technology was used to design sgRNA; Trp53 knockout mice were obtained by applying high-throughput electroporation of fertilized eggs. After sexual maturity, sperm were collected for cryopreservation.
Trp53-flox
Product ID:
S-CKO-06451
Strain:
C57BL/6NCya
Status:
Description:
Trp53 is located on chromosome 11 of mice. SgRNA and ssDNA will be designed using Nuclease Technology; Trp53 conditional knockout mice will be obtained by high-throughput electroporation of fertilized eggs. After sexual maturity, sperm will be collected for cryopreservation.
Trp53 is located on chromosome 11 of mice. SgRNA and ssDNA will be designed using Nuclease Technology; Trp53 conditional knockout mice will be obtained by high-throughput electroporation of fertilized eggs. After sexual maturity, sperm will be collected for cryopreservation.
Trp53-flox
Product ID:
S-CKO-06450
Strain:
C57BL/6JCya
Status:
Description:
Trp53 is located on chromosome 11 of mice. SgRNA and ssDNA were designed using Nuclease Technology; Trp53 conditional knockout mice were obtained by high-throughput electroporation of fertilized eggs. After sexual maturity, sperm were collected for cryopreservation.
Trp53 is located on chromosome 11 of mice. SgRNA and ssDNA were designed using Nuclease Technology; Trp53 conditional knockout mice were obtained by high-throughput electroporation of fertilized eggs. After sexual maturity, sperm were collected for cryopreservation.
Trp53-flox
Product ID:
S-CKO-06449
Strain:
C57BL/6JCya
Status:
Description:
Trp53 is located on chromosome 11 of mice. SgRNA and ssDNA were designed using Nuclease Technology; Trp53 conditional knockout mice were obtained by high-throughput electroporation of fertilized eggs. After sexual maturity, sperm were collected for cryopreservation.
Trp53 is located on chromosome 11 of mice. SgRNA and ssDNA were designed using Nuclease Technology; Trp53 conditional knockout mice were obtained by high-throughput electroporation of fertilized eggs. After sexual maturity, sperm were collected for cryopreservation.
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