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NeoBiotechnologies
CHEK2 Monoclonal Antibody (PCRP-CHEK2-1A4)
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产品信息
11200-MSM3-P1
应用
建议稀释比
已发表文章
产品规格
种属反应
Human
宿主/亚型
Mouse
/ IgG2b
分类
Monoclonal
类型
Antibody
克隆号
PCRP-CHEK2-1A4
抗原
Recombinant fragment of human CHEK2 corresponding to protein domain
偶联物
形式
Liquid
浓度
200 µg/mL
纯化类型
Protein A/G
保存液
PBS with 0.05% BSA
内含物
0.05% sodium azide
保存条件
4°C
运输条件
Ambient (domestic); Wet ice (international)
产品详细信息
Antibody is stable for 24 months.
Positive Control: HeLa or HCT 116cells.Human testis, spleen or colon. Cellular Localization: Nucleus.
Specificity Comments: Recognizes a serine/threonine protein kinase that is a required check-point to mediate cell cycle arrest, activation of DNA repair and apoptosis.In response to DNA damage and replication blocks, cell cycle progression is halted through the control of critical cell cycle regulators. The protein encoded by this gene is a cell cycle checkpoint regulator and putative tumor suppressor. It contains a forkhead-associated protein interaction domain essential for activation in response to DNA damage and is rapidly phosphorylated in response to replication blocks and DNA damage. When activated, the encoded protein is known to inhibit CDC25C phosphatase, preventing entry into mitosis, and has been shown to stabilize the tumor suppressor protein p53, leading to cell cycle arrest in G1. Also, this protein interacts with and phosphorylates BRCA1, allowing BRCA1 to restore survival after DNA damage. Mutations in this gene have been linked with Li-Fraumeni syndrome, a highly penetrant familial cancer phenotype usually associated with inherited mutations in TP53. Mutations in this gene are thought to confer a predisposition to sarcomas, breast cancer, and brain tumors.
Predicted to react with Mouse and Rat
靶标信息
CHEK2 (CHK2) is a serine/threonine kinase and a component of the DNA damage checkpoint pathway. A mutation in CHK2 has been linked to cancer. CHK2 is activated by DNA damage and phosphorylates several modulators of cell cycle control including tumor suppressor proteins. In addition, Chk2 can phosphorylate BRCA1, allowing BRCA1 to restore survival after DNA damage. Chk2 is a putative tumor suppressor protein, with mutations in to the Chk2 gene linked to Li-Fraumeni syndrome, a familiar cancer usually associated with inherited mutations in TP53. Also, mutations in CHK2 are thought to confer a predisposition to sarcomas, breast cancer, and brain tumors.
仅用于科研。不用于诊断过程。未经明确授权不得转售。
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生物信息学
蛋白别名: Cds1 homolog; Checkpoint kinase 2; Checkpoint like protein CHK2; checkpoint-like protein CHK2; Chk2 (phospho T68); Chk2 (pThr68); CHK2 checkpoint homolog; CHK2 checkpoint homolog (S. pombe); Chk2 phospho; Chk2 phospho T68; del9; EC 2.7.11.1; HuCds 1; Hucds1; kinase Chk2; OTTHUMP00000199044; OTTHUMP00000199045; OTTHUMP00000199064; OTTHUMP00000199115; OTTHUMP00000199116; phospho Chk2 (T68); phospho Thr68 Chk2; RP11-436C9.1; Serine/threonine protein kinase Chk2; Serine/threonine-protein kinase Chk2
基因别名: CDS1; CHEK2; CHK2; hCds1; HuCds1; LFS2; PP1425; RAD53
UniProt ID: (Human) O96017
Entrez Gene ID: (Human) 11200
DNA damage checkpoint
G2/M transition of mitotic cell cycle
replicative cell aging
positive regulation of protein phosphorylation
double-strand break repair
transcription, DNA-templated
regulation of transcription, DNA-templated
protein phosphorylation
cellular response to DNA damage stimulus
DNA damage induced protein phosphorylation
DNA damage response, signal transduction by p53 class mediator resulting in cell cycle arrest
intrinsic apoptotic signaling pathway in response to DNA damage
response to gamma radiation
peptidyl-serine phosphorylation
cellular response to drug
regulation of protein catabolic process
signal transduction in response to DNA damage
cellular protein catabolic process
positive regulation of transcription, DNA-templated
protein autophosphorylation
protein stabilization
cell division
negative regulation of cell cycle arrest
signal transduction involved in intra-S DNA damage checkpoint
mitotic spindle assembly
replicative senescence
regulation of signal transduction by p53 class mediator
response to doxorubicin
cellular response to bisphenol A
negative regulation of DNA damage checkpoint
positive regulation of anoikis
