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LSL-K-ras G12C
Product ID:
C001409
Strain:
C57BL/6JCya
Status:
Description:
The Kirsten rat sarcoma viral oncogene homolog (KRAS) is a proto-oncogene encoding the K-Ras protein, a membrane-associated GTPase, and a key member of the RAS gene family. K-Ras protein plays a crucial role in the RAS/MAPK signaling pathway by regulating the interconversion between GTP and GDP, transmitting extracellular signals to the nucleus, and thus influencing cell growth, proliferation, and differentiation [1]. KRAS is among the most frequently mutated genes in cancer, with mutations at codons 12, 13, and 61 leading to constitutive activation of the K-Ras protein. These alterations interact with multiple effector molecules and activate downstream signaling pathways, resulting in uncontrolled cellular proliferation and oncogenesis [2]. Approximately 30% of cancer patients harbor KRAS mutations. Specifically, 90% of pancreatic cancers, 50% of colorectal cancers, 25% of lung cancers, and 20–30% of non-small cell lung cancers (NSCLC) exhibit KRAS mutations. The G12C mutation is one of the most common KRAS mutations, accounting for 33% of all KRAS mutations, and is particularly prevalent in NSCLC. The G12C mutation is also present in approximately 14% of pancreatic cancers, 3–4% of colorectal cancers, and 1–2% of cholangiocarcinomas [3].
This strain is a conditional expression model of K-ras G12C, generated by introducing the G12C point mutation into the mouse Kras gene. Under normal conditions, the expression of K-ras G12C is blocked by an upstream loxP-Stop-loxP cassette. Expression is achieved only upon crossing with Cre mice, where Cre recombinase-mediated loxP site recombination removes the blocking sequence. This enables precise temporal and spatial control of K-ras G12C expression and tumorigenesis. By mating with tissue-specific Cre mice, this model can conditionally express K-ras G12C in specific tissues, making it a valuable tool for constructing cancer models in various tissues and organs. Homozygous LSL-K-ras G12C mice are nonviable.
This strain is a conditional expression model of K-ras G12C, generated by introducing the G12C point mutation into the mouse Kras gene. Under normal conditions, the expression of K-ras G12C is blocked by an upstream loxP-Stop-loxP cassette. Expression is achieved only upon crossing with Cre mice, where Cre recombinase-mediated loxP site recombination removes the blocking sequence. This enables precise temporal and spatial control of K-ras G12C expression and tumorigenesis. By mating with tissue-specific Cre mice, this model can conditionally express K-ras G12C in specific tissues, making it a valuable tool for constructing cancer models in various tissues and organs. Homozygous LSL-K-ras G12C mice are nonviable.
The Kirsten rat sarcoma viral oncogene homolog (KRAS) is a proto-oncogene encoding the K-Ras protein, a membrane-associated GTPase, and a key member of the RAS gene family. K-Ras protein plays a crucial role in the RAS/MAPK signaling pathway by regulating the interconversion between GTP and GDP, transmitting extracellular signals to the nucleus, and thus influencing cell growth, proliferation, and differentiation [1]. KRAS is among the most frequently mutated genes in cancer, with mutations at codons 12, 13, and 61 leading to constitutive activation of the K-Ras protein. These alterations interact with multiple effector molecules and activate downstream signaling pathways, resulting in uncontrolled cellular proliferation and oncogenesis [2]. Approximately 30% of cancer patients harbor KRAS mutations. Specifically, 90% of pancreatic cancers, 50% of colorectal cancers, 25% of lung cancers, and 20–30% of non-small cell lung cancers (NSCLC) exhibit KRAS mutations. The G12C mutation is one of the most common KRAS mutations, accounting for 33% of all KRAS mutations, and is particularly prevalent in NSCLC. The G12C mutation is also present in approximately 14% of pancreatic cancers, 3–4% of colorectal cancers, and 1–2% of cholangiocarcinomas [3].
This strain is a conditional expression model of K-ras G12C, generated by introducing the G12C point mutation into the mouse Kras gene. Under normal conditions, the expression of K-ras G12C is blocked by an upstream loxP-Stop-loxP cassette. Expression is achieved only upon crossing with Cre mice, where Cre recombinase-mediated loxP site recombination removes the blocking sequence. This enables precise temporal and spatial control of K-ras G12C expression and tumorigenesis. By mating with tissue-specific Cre mice, this model can conditionally express K-ras G12C in specific tissues, making it a valuable tool for constructing cancer models in various tissues and organs. Homozygous LSL-K-ras G12C mice are nonviable.
This strain is a conditional expression model of K-ras G12C, generated by introducing the G12C point mutation into the mouse Kras gene. Under normal conditions, the expression of K-ras G12C is blocked by an upstream loxP-Stop-loxP cassette. Expression is achieved only upon crossing with Cre mice, where Cre recombinase-mediated loxP site recombination removes the blocking sequence. This enables precise temporal and spatial control of K-ras G12C expression and tumorigenesis. By mating with tissue-specific Cre mice, this model can conditionally express K-ras G12C in specific tissues, making it a valuable tool for constructing cancer models in various tissues and organs. Homozygous LSL-K-ras G12C mice are nonviable.
Kras-KO
Product ID:
S-KO-02814
Strain:
C57BL/6JCya
Status:
Description:
Kras is located on chromosome 6 of mice. Nuclease Technology was used to design sgRNA; Kras knockout mice were obtained by applying high-throughput electroporation of fertilized eggs. After sexual maturity, sperm were collected for cryopreservation.
Kras is located on chromosome 6 of mice. Nuclease Technology was used to design sgRNA; Kras knockout mice were obtained by applying high-throughput electroporation of fertilized eggs. After sexual maturity, sperm were collected for cryopreservation.
KS (inducible)
Product ID:
C001514
Strain:
C57BL/6JCya
Status:
Description:
KRAS is an oncogene that encodes the K-Ras protein, a key component of the RAS/MAPK signaling pathway. The K-Ras protein plays an important regulatory role in various cellular processes, including cell growth, proliferation, maturation, and differentiation. KRAS gene mutations are a common cause of cancer, with approximately 30% of cancer patients harboring KRAS mutations. These mutations are predominantly single-nucleotide missense mutations, with over 80% occurring at the 12th amino acid residue (G12), particularly the KRAS G12D mutation, which is very common in lung and pancreatic cancers. The G12D mutation enhances the activity of the K-Ras protein, leading to uncontrolled cell growth and division, thereby promoting tumor formation. The K-Ras protein is highly conserved between mice and humans, with only differences at the 132nd and 187th amino acid residues[1-2].
The SFTPC gene encodes surfactant protein C (SP-C), one of the four major proteins that make up surfactant. Surfactant is a mixture of lipids and proteins that coats the surface of lung tissue, reducing respiratory resistance. It is produced and secreted by alveolar cells, and its main function is to maintain the stability of lung tissue by reducing the surface tension of lung fluid. In addition, SP-C protein is involved in lung development and function, including alveolar formation, airway remodeling, and immune defense. The SFTPC gene is expressed primarily in the lung, with the highest expression in the lower lobes, right lung, upper lobes, left upper lobes, and visceral pleura. It is also expressed at lower levels in other tissues. Type II alveolar cells are the main producers and secretors of surfactants, and the SFTPC gene is highly expressed in these cells, making it a specific marker of this cell type.
The KS (inducible) mouse is an induced lung cancer model that is constructed by crossing LSL-K-ras G12D mice (Catalog number: C001064), a conditional over-expressing K-Ras G12D mutant gene mouse strain, and Sftpc-MerCreMer mice (Catalog number: C001501), a type II alveolar cell-specific Cre recombinase expressing mouse strain, and then inducing with tamoxifen. Tamoxifen can trigger sequence recombination between loxP sites mediated by Cre recombinase in the type II alveolar cells of the offspring mice, resulting in the specific deletion of the Loxp-Stop-Loxp (LSL) gene silencing element in the type II alveolar cells, thereby enabling the K-Ras G12D mutant gene to be selectively expressed in the lung tissue. Internal data indicates that the model may exhibit slight expression leakage in the absence of tamoxifen induction, leading to the occurrence of a small number of pulmonary adenomas.
KRAS is an oncogene that encodes the K-Ras protein, a key component of the RAS/MAPK signaling pathway. The K-Ras protein plays an important regulatory role in various cellular processes, including cell growth, proliferation, maturation, and differentiation. KRAS gene mutations are a common cause of cancer, with approximately 30% of cancer patients harboring KRAS mutations. These mutations are predominantly single-nucleotide missense mutations, with over 80% occurring at the 12th amino acid residue (G12), particularly the KRAS G12D mutation, which is very common in lung and pancreatic cancers. The G12D mutation enhances the activity of the K-Ras protein, leading to uncontrolled cell growth and division, thereby promoting tumor formation. The K-Ras protein is highly conserved between mice and humans, with only differences at the 132nd and 187th amino acid residues[1-2].
The SFTPC gene encodes surfactant protein C (SP-C), one of the four major proteins that make up surfactant. Surfactant is a mixture of lipids and proteins that coats the surface of lung tissue, reducing respiratory resistance. It is produced and secreted by alveolar cells, and its main function is to maintain the stability of lung tissue by reducing the surface tension of lung fluid. In addition, SP-C protein is involved in lung development and function, including alveolar formation, airway remodeling, and immune defense. The SFTPC gene is expressed primarily in the lung, with the highest expression in the lower lobes, right lung, upper lobes, left upper lobes, and visceral pleura. It is also expressed at lower levels in other tissues. Type II alveolar cells are the main producers and secretors of surfactants, and the SFTPC gene is highly expressed in these cells, making it a specific marker of this cell type.
The KS (inducible) mouse is an induced lung cancer model that is constructed by crossing LSL-K-ras G12D mice (Catalog number: C001064), a conditional over-expressing K-Ras G12D mutant gene mouse strain, and Sftpc-MerCreMer mice (Catalog number: C001501), a type II alveolar cell-specific Cre recombinase expressing mouse strain, and then inducing with tamoxifen. Tamoxifen can trigger sequence recombination between loxP sites mediated by Cre recombinase in the type II alveolar cells of the offspring mice, resulting in the specific deletion of the Loxp-Stop-Loxp (LSL) gene silencing element in the type II alveolar cells, thereby enabling the K-Ras G12D mutant gene to be selectively expressed in the lung tissue. Internal data indicates that the model may exhibit slight expression leakage in the absence of tamoxifen induction, leading to the occurrence of a small number of pulmonary adenomas.
Kras-flox
Product ID:
S-CKO-03297
Strain:
C57BL/6JCya
Status:
Description:
Kras is located on chromosome 6 of mice. SgRNA and ssDNA were designed using Nuclease Technology; Kras conditional knockout mice were obtained by high-throughput electroporation of fertilized eggs. After sexual maturity, sperm were collected for cryopreservation.
Kras is located on chromosome 6 of mice. SgRNA and ssDNA were designed using Nuclease Technology; Kras conditional knockout mice were obtained by high-throughput electroporation of fertilized eggs. After sexual maturity, sperm were collected for cryopreservation.
Rosa26-hHRAS
Product ID:
I001213
Strain:
C57BL/6JCya
Status:
Description:
The HRas oncogene (HRAS), also known as the Harvey Rat Sarcoma Viral Oncogene Homolog (HRAS), is a member of the Ras oncogene family, which also includes KRAS and NRAS. All members of this family are associated with the development of mammalian sarcoma retroviruses [1]. HRAS encodes the H-Ras protein, a small GTPase responsible for transmitting signals from cell surface receptors to the nucleus, regulating cell proliferation, survival, and differentiation. HRAS is primarily expressed in various tissues, including the brain, heart, and skeletal muscle, and is involved in controlling the cellular response to growth factors. As a member of the small GTPase family, HRAS acts as a molecular switch, cycling between active and inactive states to influence key cellular processes. Mutations in the HRAS gene can lead to abnormal signal transduction, commonly found in tumors of stratified epithelial tissues, such as bladder cancer, thyroid cancer, and head and neck squamous cell carcinoma. Additionally, HRAS is associated with Costello syndrome, a genetic disorder characterized by developmental delays and an increased risk of tumors [2-3].
Early studies have shown that genotoxic carcinogens shorten the latency period and increase the incidence of malignant tumors in rasH2 mice, which carry the human HRAS (c-Ha-ras) oncogene, compared to non-transgenic mice. Therefore, rasH2 mice are ideal animal models for rapid carcinogenicity testing [4-5]. Further research has shown that F1 hybrid mice (CB6F1 background rasH2 mice) obtained by mating male C57BL/6J mice carrying the human prototype c-Ha-ras gene with female BALB/c mice are significantly more sensitive to both mutagenic and non-mutagenic carcinogens than control mice [5]. These mice are highly sensitive to the carcinogenicity of both genotoxic and non-genotoxic compounds while showing no response to non-carcinogens [6]. Between 12 to 18 months of age, rasH2 mice primarily develop spontaneous alveolar adenomas/bronchial adenomas/adenocarcinomas, splenic hemangiomas/hemangiosarcomas, and a smaller number of skin and gastric papillomas and lymphomas [4]. In the 1990s, this mouse model was officially approved by the FDA for carcinogenicity evaluations in drug safety assessments, reducing the standard two-year carcinogenicity test in common rodents to six months.
The Rosa26-hHRAS mouse model is a humanized model constructed by integrating a human HRAS gene with the c.450+180A>G mutation into the Rosa26 safe harbor site in mice using gene editing technology. The introduction of the c.450+180A>G mutation significantly enhances HRAS gene expression. This model can be used for rapid in vivo testing of the carcinogenicity of genotoxic and non-genotoxic compounds, studying the impact of HRAS oncogene point mutations on tumorigenesis and development, and developing tumor prevention or suppression therapies.
The HRas oncogene (HRAS), also known as the Harvey Rat Sarcoma Viral Oncogene Homolog (HRAS), is a member of the Ras oncogene family, which also includes KRAS and NRAS. All members of this family are associated with the development of mammalian sarcoma retroviruses [1]. HRAS encodes the H-Ras protein, a small GTPase responsible for transmitting signals from cell surface receptors to the nucleus, regulating cell proliferation, survival, and differentiation. HRAS is primarily expressed in various tissues, including the brain, heart, and skeletal muscle, and is involved in controlling the cellular response to growth factors. As a member of the small GTPase family, HRAS acts as a molecular switch, cycling between active and inactive states to influence key cellular processes. Mutations in the HRAS gene can lead to abnormal signal transduction, commonly found in tumors of stratified epithelial tissues, such as bladder cancer, thyroid cancer, and head and neck squamous cell carcinoma. Additionally, HRAS is associated with Costello syndrome, a genetic disorder characterized by developmental delays and an increased risk of tumors [2-3].
Early studies have shown that genotoxic carcinogens shorten the latency period and increase the incidence of malignant tumors in rasH2 mice, which carry the human HRAS (c-Ha-ras) oncogene, compared to non-transgenic mice. Therefore, rasH2 mice are ideal animal models for rapid carcinogenicity testing [4-5]. Further research has shown that F1 hybrid mice (CB6F1 background rasH2 mice) obtained by mating male C57BL/6J mice carrying the human prototype c-Ha-ras gene with female BALB/c mice are significantly more sensitive to both mutagenic and non-mutagenic carcinogens than control mice [5]. These mice are highly sensitive to the carcinogenicity of both genotoxic and non-genotoxic compounds while showing no response to non-carcinogens [6]. Between 12 to 18 months of age, rasH2 mice primarily develop spontaneous alveolar adenomas/bronchial adenomas/adenocarcinomas, splenic hemangiomas/hemangiosarcomas, and a smaller number of skin and gastric papillomas and lymphomas [4]. In the 1990s, this mouse model was officially approved by the FDA for carcinogenicity evaluations in drug safety assessments, reducing the standard two-year carcinogenicity test in common rodents to six months.
The Rosa26-hHRAS mouse model is a humanized model constructed by integrating a human HRAS gene with the c.450+180A>G mutation into the Rosa26 safe harbor site in mice using gene editing technology. The introduction of the c.450+180A>G mutation significantly enhances HRAS gene expression. This model can be used for rapid in vivo testing of the carcinogenicity of genotoxic and non-genotoxic compounds, studying the impact of HRAS oncogene point mutations on tumorigenesis and development, and developing tumor prevention or suppression therapies.
2*hHRAS(CB6F1)
Product ID:
C001643
Strain:
BALB/c;B6JCya
Status:
Description:
The HRas oncogene (HRAS), also known as the Harvey Rat Sarcoma Viral Oncogene Homolog (HRAS), is a member of the Ras oncogene family, which also includes KRAS and NRAS. All members of this family are associated with the development of mammalian sarcoma retroviruses [1]. HRAS encodes the H-Ras protein, a small GTPase responsible for transmitting signals from cell surface receptors to the nucleus, regulating cell proliferation, survival, and differentiation. HRAS is primarily expressed in various tissues, including the brain, heart, and skeletal muscle, and is involved in controlling the cellular response to growth factors. As a member of the small GTPase family, HRAS acts as a molecular switch, cycling between active and inactive states to influence key cellular processes. Mutations in the HRAS gene can lead to abnormal signal transduction, commonly found in tumors of stratified epithelial tissues, such as bladder cancer, thyroid cancer, and head and neck squamous cell carcinoma. Additionally, HRAS is associated with Costello syndrome, a genetic disorder characterized by developmental delays and an increased risk of tumors [2-3].
Early studies have shown that genotoxic carcinogens shorten the latency period and increase the incidence of malignant tumors in rasH2 mice, which carry the human HRAS (c-Ha-ras) oncogene, compared to non-transgenic mice. Therefore, rasH2 mice are ideal animal models for rapid carcinogenicity testing [4-5]. Further research has shown that F1 hybrid mice (CB6F1 background rasH2 mice) obtained by mating male C57BL/6J mice carrying the human prototype c-Ha-ras gene with female BALB/c mice are significantly more sensitive to both mutagenic and non-mutagenic carcinogens than control mice [5]. These mice are highly sensitive to the carcinogenicity of both genotoxic and non-genotoxic compounds while showing no response to non-carcinogens [6]. Between 12 to 18 months of age, rasH2 mice primarily develop spontaneous alveolar adenomas/bronchial adenomas/adenocarcinomas, splenic hemangiomas/hemangiosarcomas, and a smaller number of skin and gastric papillomas and lymphomas [4]. In the 1990s, this mouse model was officially approved by the FDA for carcinogenicity evaluations in drug safety assessments, reducing the standard two-year carcinogenicity test in common rodents to six months.
The 2*hHRAS(CB6F1) mouse was obtained by mating double-genotype B6-Rosa26-hHRAS[KI/+]; H11-hHRAS[KI/+] mice with BALB/cAnCya mice. The double-genotype B6-Rosa26-hHRAS[KI/+]; H11-hHRAS[KI/+] mice were generated by crossing Rosa26-hHRAS mice (Catalog No.: I001213) with H11-hHRAS mice, both on the C57BL/6JCya background. This model carries two copies of the human proto-oncogene c-Ha-ras on a C57BL/6J × BALB/c hybrid background (i.e., CB6F1 background) and exhibits increased sensitivity to both genotoxic and non-genotoxic human carcinogens. 2*hHRAS(CB6F1) mice can be used for rapid in vivo testing of the carcinogenicity of genotoxic and non-genotoxic compounds, studying the impact of HRAS oncogene point mutations on tumorigenesis and development, and developing tumor prevention or suppression therapies.
The HRas oncogene (HRAS), also known as the Harvey Rat Sarcoma Viral Oncogene Homolog (HRAS), is a member of the Ras oncogene family, which also includes KRAS and NRAS. All members of this family are associated with the development of mammalian sarcoma retroviruses [1]. HRAS encodes the H-Ras protein, a small GTPase responsible for transmitting signals from cell surface receptors to the nucleus, regulating cell proliferation, survival, and differentiation. HRAS is primarily expressed in various tissues, including the brain, heart, and skeletal muscle, and is involved in controlling the cellular response to growth factors. As a member of the small GTPase family, HRAS acts as a molecular switch, cycling between active and inactive states to influence key cellular processes. Mutations in the HRAS gene can lead to abnormal signal transduction, commonly found in tumors of stratified epithelial tissues, such as bladder cancer, thyroid cancer, and head and neck squamous cell carcinoma. Additionally, HRAS is associated with Costello syndrome, a genetic disorder characterized by developmental delays and an increased risk of tumors [2-3].
Early studies have shown that genotoxic carcinogens shorten the latency period and increase the incidence of malignant tumors in rasH2 mice, which carry the human HRAS (c-Ha-ras) oncogene, compared to non-transgenic mice. Therefore, rasH2 mice are ideal animal models for rapid carcinogenicity testing [4-5]. Further research has shown that F1 hybrid mice (CB6F1 background rasH2 mice) obtained by mating male C57BL/6J mice carrying the human prototype c-Ha-ras gene with female BALB/c mice are significantly more sensitive to both mutagenic and non-mutagenic carcinogens than control mice [5]. These mice are highly sensitive to the carcinogenicity of both genotoxic and non-genotoxic compounds while showing no response to non-carcinogens [6]. Between 12 to 18 months of age, rasH2 mice primarily develop spontaneous alveolar adenomas/bronchial adenomas/adenocarcinomas, splenic hemangiomas/hemangiosarcomas, and a smaller number of skin and gastric papillomas and lymphomas [4]. In the 1990s, this mouse model was officially approved by the FDA for carcinogenicity evaluations in drug safety assessments, reducing the standard two-year carcinogenicity test in common rodents to six months.
The 2*hHRAS(CB6F1) mouse was obtained by mating double-genotype B6-Rosa26-hHRAS[KI/+]; H11-hHRAS[KI/+] mice with BALB/cAnCya mice. The double-genotype B6-Rosa26-hHRAS[KI/+]; H11-hHRAS[KI/+] mice were generated by crossing Rosa26-hHRAS mice (Catalog No.: I001213) with H11-hHRAS mice, both on the C57BL/6JCya background. This model carries two copies of the human proto-oncogene c-Ha-ras on a C57BL/6J × BALB/c hybrid background (i.e., CB6F1 background) and exhibits increased sensitivity to both genotoxic and non-genotoxic human carcinogens. 2*hHRAS(CB6F1) mice can be used for rapid in vivo testing of the carcinogenicity of genotoxic and non-genotoxic compounds, studying the impact of HRAS oncogene point mutations on tumorigenesis and development, and developing tumor prevention or suppression therapies.
BALB/c;B6J-Rosa26-hHRAS
Product ID:
I001214
Strain:
BALB/c;B6JCya
Status:
Description:
The HRas oncogene (HRAS), also known as the Harvey Rat Sarcoma Viral Oncogene Homolog (HRAS), is a member of the Ras oncogene family, which also includes KRAS and NRAS. All members of this family are associated with the development of mammalian sarcoma retroviruses [1]. HRAS encodes the H-Ras protein, a small GTPase responsible for transmitting signals from cell surface receptors to the nucleus, regulating cell proliferation, survival, and differentiation. HRAS is primarily expressed in various tissues, including the brain, heart, and skeletal muscle, and is involved in controlling the cellular response to growth factors. As a member of the small GTPase family, HRAS acts as a molecular switch, cycling between active and inactive states to influence key cellular processes. Mutations in the HRAS gene can lead to abnormal signal transduction, commonly found in tumors of stratified epithelial tissues, such as bladder cancer, thyroid cancer, and head and neck squamous cell carcinoma. Additionally, HRAS is associated with Costello syndrome, a genetic disorder characterized by developmental delays and an increased risk of tumors [2-3].
Early studies have shown that genotoxic carcinogens shorten the latency period and increase the incidence of malignant tumors in rasH2 mice, which carry the human HRAS (c-Ha-ras) oncogene, compared to non-transgenic mice. Therefore, rasH2 mice are ideal animal models for rapid carcinogenicity testing [4-5]. Further research has shown that F1 hybrid mice (CB6F1 background rasH2 mice) obtained by mating male C57BL/6J mice carrying the human prototype c-Ha-ras gene with female BALB/c mice are significantly more sensitive to both mutagenic and non-mutagenic carcinogens than control mice [5]. These mice are highly sensitive to the carcinogenicity of both genotoxic and non-genotoxic compounds while showing no response to non-carcinogens [6]. Between 12 to 18 months of age, rasH2 mice primarily develop spontaneous alveolar adenomas/bronchial adenomas/adenocarcinomas, splenic hemangiomas/hemangiosarcomas, and a smaller number of skin and gastric papillomas and lymphomas [4]. In the 1990s, this mouse model was officially approved by the FDA for carcinogenicity evaluations in drug safety assessments, reducing the standard two-year carcinogenicity test in common rodents to six months.
BALB/c;B6J-Rosa26-hHRAS mice are obtained by crossing Rosa26-hHRAS mice on a C57BL/6JCya background (Catalog No.: I001213) with BALB/cAnCya mice. This hybrid strain exhibits higher sensitivity to both genotoxic and non-genotoxic human carcinogens. BALB/c;B6J-Rosa26-hHRAS mice can be used for rapid in vivo testing of the carcinogenicity of genotoxic and non-genotoxic compounds, studying the impact of HRAS oncogene point mutations on tumorigenesis and development, and developing tumor prevention or suppression therapies.
The HRas oncogene (HRAS), also known as the Harvey Rat Sarcoma Viral Oncogene Homolog (HRAS), is a member of the Ras oncogene family, which also includes KRAS and NRAS. All members of this family are associated with the development of mammalian sarcoma retroviruses [1]. HRAS encodes the H-Ras protein, a small GTPase responsible for transmitting signals from cell surface receptors to the nucleus, regulating cell proliferation, survival, and differentiation. HRAS is primarily expressed in various tissues, including the brain, heart, and skeletal muscle, and is involved in controlling the cellular response to growth factors. As a member of the small GTPase family, HRAS acts as a molecular switch, cycling between active and inactive states to influence key cellular processes. Mutations in the HRAS gene can lead to abnormal signal transduction, commonly found in tumors of stratified epithelial tissues, such as bladder cancer, thyroid cancer, and head and neck squamous cell carcinoma. Additionally, HRAS is associated with Costello syndrome, a genetic disorder characterized by developmental delays and an increased risk of tumors [2-3].
Early studies have shown that genotoxic carcinogens shorten the latency period and increase the incidence of malignant tumors in rasH2 mice, which carry the human HRAS (c-Ha-ras) oncogene, compared to non-transgenic mice. Therefore, rasH2 mice are ideal animal models for rapid carcinogenicity testing [4-5]. Further research has shown that F1 hybrid mice (CB6F1 background rasH2 mice) obtained by mating male C57BL/6J mice carrying the human prototype c-Ha-ras gene with female BALB/c mice are significantly more sensitive to both mutagenic and non-mutagenic carcinogens than control mice [5]. These mice are highly sensitive to the carcinogenicity of both genotoxic and non-genotoxic compounds while showing no response to non-carcinogens [6]. Between 12 to 18 months of age, rasH2 mice primarily develop spontaneous alveolar adenomas/bronchial adenomas/adenocarcinomas, splenic hemangiomas/hemangiosarcomas, and a smaller number of skin and gastric papillomas and lymphomas [4]. In the 1990s, this mouse model was officially approved by the FDA for carcinogenicity evaluations in drug safety assessments, reducing the standard two-year carcinogenicity test in common rodents to six months.
BALB/c;B6J-Rosa26-hHRAS mice are obtained by crossing Rosa26-hHRAS mice on a C57BL/6JCya background (Catalog No.: I001213) with BALB/cAnCya mice. This hybrid strain exhibits higher sensitivity to both genotoxic and non-genotoxic human carcinogens. BALB/c;B6J-Rosa26-hHRAS mice can be used for rapid in vivo testing of the carcinogenicity of genotoxic and non-genotoxic compounds, studying the impact of HRAS oncogene point mutations on tumorigenesis and development, and developing tumor prevention or suppression therapies.
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