フィルター
6 件の結果が “11789” で取得されました
並べ替える:
アルファベット順（A-Z）
ベストセラー
Apc KO
製品ID :
C001511
系統:
C57BL/6JCya
状況:
説明:
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].
The Apc KO mouse is a research model constructed by using gene editing technology to knock out the sequence in the mouse Apc gene that contains the mutation cluster region (MCR), and this strain is homozygous lethal. Heterozygous Apc KO mice can spontaneously develop intestinal adenomas and exhibit significant colorectal cancer disease phenotypes in various aspects such as survival, growth, food intake, and intestinal lesions. Therefore, Apc KO mice can be used for familial adenomatous polyposis (FAP) and colorectal cancer and other tumors or tumor-related diseases, as well as the study of the regulatory mechanism of the Wnt/β-catenin signaling pathway.
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].
The Apc KO mouse is a research model constructed by using gene editing technology to knock out the sequence in the mouse Apc gene that contains the mutation cluster region (MCR), and this strain is homozygous lethal. Heterozygous Apc KO mice can spontaneously develop intestinal adenomas and exhibit significant colorectal cancer disease phenotypes in various aspects such as survival, growth, food intake, and intestinal lesions. Therefore, Apc KO mice can be used for familial adenomatous polyposis (FAP) and colorectal cancer and other tumors or tumor-related diseases, as well as the study of the regulatory mechanism of the Wnt/β-catenin signaling pathway.
Trp53&Apc dKO
製品ID :
C001909
系統:
C57BL/6JCya
状況:
説明:
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.
Apc-KO
製品ID :
S-KO-01083
系統:
C57BL/6JCya
状況:
説明:
Apc is located on chromosome 18 of mice. Nuclease Technology was used to design sgRNA; Apc knockout mice were obtained by applying high-throughput electroporation of fertilized eggs. After sexual maturity, sperm were collected for cryopreservation.
Apc is located on chromosome 18 of mice. Nuclease Technology was used to design sgRNA; Apc knockout mice were obtained by applying high-throughput electroporation of fertilized eggs. After sexual maturity, sperm were collected for cryopreservation.
Apc-flox
製品ID :
S-CKO-01244
系統:
C57BL/6JCya
状況:
説明:
Apc is located on chromosome 18 of mice. SgRNA and ssDNA were designed using Nuclease Technology; Apc conditional knockout mice were obtained by high-throughput electroporation of fertilized eggs. After sexual maturity, sperm were collected for cryopreservation.
Apc is located on chromosome 18 of mice. SgRNA and ssDNA were designed using Nuclease Technology; Apc conditional knockout mice were obtained by high-throughput electroporation of fertilized eggs. After sexual maturity, sperm were collected for cryopreservation.
Esf1-KO
製品ID :
S-KO-11789
系統:
C57BL/6JCya
状況:
説明:
Esf1 is located on chromosome 2 of mice. Nuclease Technology will be used to design sgRNA; Esf1 knockout mice will be obtained by applying high-throughput electroporation of fertilized eggs. After sexual maturity, sperm were collected for cryopreservation.
Esf1 is located on chromosome 2 of mice. Nuclease Technology will be used to design sgRNA; Esf1 knockout mice will be obtained by applying high-throughput electroporation of fertilized eggs. After sexual maturity, sperm were collected for cryopreservation.
Hpse2-flox
製品ID :
S-CKO-11789
系統:
C57BL/6JCya
状況:
説明:
Hpse2 is located on chromosome 19 of mice. SgRNA and ssDNA will be designed using Nuclease Technology; Hpse2 conditional knockout mice will be obtained by high-throughput electroporation of fertilized eggs. After sexual maturity, sperm will be collected for cryopreservation.
Hpse2 is located on chromosome 19 of mice. SgRNA and ssDNA will be designed using Nuclease Technology; Hpse2 conditional knockout mice will be obtained by high-throughput electroporation of fertilized eggs. After sexual maturity, sperm will be collected for cryopreservation.
Items: 1 to 6 of 6
1