FITC标记的磷酸化细胞周期检测点激酶2抗体
产品名称： FITC标记的磷酸化细胞周期检测点激酶2抗体
英文名称： Anti-Phospho-CHK2 (Thr383)/FITC
产品编号： HZ-13910R-FITC
产品价格： null
产品产地： 中国/上海
品牌商标： HZbscience
更新时间： 2023-08-17T10:24:20
使用范围： ICC=1:50-200 IF=1:50-200
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Rabbit Anti-Phospho-CHK2 (Thr383)/FITC Conjugated antibody
FITC标记的磷酸化细胞周期检测点激酶2抗体
| 英文名称 | Anti-Phospho-CHK2 (Thr383)/FITC |
| 中文名称 | FITC标记的磷酸化细胞周期检测点激酶2抗体 |
| 别 名 | Chk2 (phospho T383); p-Chk2 (phospho T383); bA444G7; CHK2 checkpoint homolog; CHK2_HUMAN; Serine/threonine-protein kinase Chk2; CDS 1; CDS1; Checkpoint kinase 2; Checkpoint like protein CHK2; Chek 2; Chek2; Chk 2; CHK2 checkpoint homolog (S. pombe); CHK2 checkpoint homolog; HuCds 1; HuCds1; LFS 2; LFS2; PP1425; RAD 53; RAD53; Rad53 homolog; Serine/threonine protein kinase Chk2. |
| 规格价格 | 100ul/2980元 购买 大包装/询价 |
| 说 明 书 | 100ul |
| 研究领域 | 肿瘤 细胞生物 信号转导 表观遗传学 |
| 抗体来源 | Rabbit |
| 克隆类型 | Polyclonal |
| 交叉反应 | Human, Dog, Pig, Cow, Horse, Sheep, |
| 产品应用 | ICC=1:50-200 IF=1:50-200 not yet tested in other applications. optimal dilutions/concentrations should be determined by the end user. |
| 分 子 量 | 61kDa |
| 性 状 | Lyophilized or Liquid |
| 浓 度 | 1mg/ml |
| 免 疫 原 | KLH conjugated Synthesised phosphopeptide derived from human CHK2 around the phosphorylation site of Thr383 |
| 亚 型 | IgG |
| 纯化方法 | affinity purified by Protein A |
| 储 存 液 | 0.01M TBS(pH7.4) with 1% BSA, 0.03% Proclin300 and 50% Glycerol. |
| 保存条件 | Store at -20 °C for one year. Avoid repeated freeze/thaw cycles. The lyophilized antibody is stable at room temperature for at least one month and for greater than a year when kept at -20°C. When reconstituted in sterile pH 7.4 0.01M PBS or diluent of antibody the antibody is stable for at least two weeks at 2-4 °C. |
| 产品介绍 | background: 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. In addition, 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. Also, mutations in this gene are thought to confer a predisposition to sarcomas, breast cancer, and brain tumors. This nuclear protein is a member of the CDS1 subfamily of serine/threonine protein kinases. Several transcript variants encoding different isoforms have been found for this gene. [provided by RefSeq, Apr 2012] Function: Serine/threonine-protein kinase which is required for checkpoint-mediated cell cycle arrest, activation of DNA repair and apoptosis in response to the presence of DNA double-strand breaks. May also negatively regulate cell cycle progression during unperturbed cell cycles. Following activation, phosphorylates numerous effectors preferentially at the consensus sequence [L-X-R-X-X-S/T]. Regulates cell cycle checkpoint arrest through phosphorylation of CDC25A, CDC25B and CDC25C, inhibiting their activity. Inhibition of CDC25 phosphatase activity leads to increased inhibitory tyrosine phosphorylation of CDK-cyclin complexes and blocks cell cycle progression. May also phosphorylate NEK6 which is involved in G2/M cell cycle arrest. Regulates DNA repair through phosphorylation of BRCA2, enhancing the association of RAD51 with chromatin which promotes DNA repair by homologous recombination. Also stimulates the transcription of genes involved in DNA repair (including BRCA2) through the phosphorylation and activation of the transcription factor FOXM1. Regulates apoptosis through the phosphorylation of p53/TP53, MDM4 and PML. Phosphorylation of p53/TP53 at 'Ser-20' by CHEK2 may alleviate inhibition by MDM2, leading to accumulation of active p53/TP53. Phosphorylation of MDM4 may also reduce degradation of p53/TP53. Also controls the transcription of pro-apoptotic genes through phosphorylation of the transcription factor E2F1. Tumor suppressor, it may also have a DNA damage-independent function in mitotic spindle assembly by phosphorylating BRCA1. Its absence may be a cause of the chromosomal instability observed in some cancer cells. Subunit: Homodimer. Homodimerization is part of the activation process but the dimer may dissociate following activation. Interacts with PML. Interacts with TP53. Interacts with RB1; phosphorylates RB1. Interacts with BRCA1. Interacts (phosphorylated at Thr-68) with MDC1; requires ATM-mediated phosphorylation of CHEK2. Interacts with TP53BP1; modulates CHEK2 phosphorylation at Thr-68 in response to ionizing radiation. Interacts with CDC25A; phosphorylates CDC25A and mediates its degradation in response to ionizing radiation. Interacts with CUL1; mediates CHEK2 ubiquitination and regulation. Subcellular Location : Isoform 2: Nucleus. Note=Isoform 10 is present throughout the cell. Subcellular Location: Nucleus; Nucleus. Isoform 10 is present throughout the cell and Nucleus; PML body. Nucleus; nucleoplasm. Recruited into PML bodies together with TP53. Tissue Specificity: High expression is found in testis, spleen, colon and peripheral blood leukocytes. Low expression is found in other tissues. Post-translational modifications: Phosphorylated. Phosphorylated at Ser-73 by PLK3 in response to DNA damage, promoting phosphorylation at Thr-68 by ATM and the G2/M transition checkpoint. Phosphorylation at Thr-68 induces homodimerization. Autophosphorylates at Thr-383 and Thr-387 in the T-loop/activation segment upon dimerization to become fully active and phosphorylate its substrates like for instance CDC25C. DNA damage-induced autophosphorylation at Ser-379 induces CUL1-mediated ubiquitination and regulates the pro-apoptotic function. Phosphorylation at Ser-456 also regulates ubiquitination. Phosphorylated by PLK4. DISEASE: Defects in CHEK2 are associated with Li-Fraumeni syndrome 2 (LFS2) [MIM:609265]; a highly penetrant familial cancer phenotype usually associated with inherited mutations in p53/TP53. Defects in CHEK2 may be a cause of susceptibility to prostate cancer (PC) [MIM:176807]. It is a malignancy originating in tissues of the prostate. Most prostate cancers are adenocarcinomas that develop in the acini of the prostatic ducts. Other rare histopathologic types of prostate cancer that occur in approximately 5% of patients include small cell carcinoma, mucinous carcinoma, prostatic ductal carcinoma, transitional cell carcinoma, squamous cell carcinoma, basal cell carcinoma, adenoid cystic carcinoma (basaloid), signet-ring cell carcinoma and neuroendocrine carcinoma. Defects in CHEK2 are found in some patients with osteogenic sarcoma (OSRC) [MIM:259500]. Similarity: Belongs to the protein kinase superfamily. CAMK Ser/Thr protein kinase family. CHK2 subfamily. Contains 1 FHA domain. Contains 1 protein kinase domain. Database links: Entrez Gene: 11200 Human Omim: 604373 Human SwissProt: O96017 Human Unigene: 291363 Human Unigene: 505297 Human Important Note: This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications |
响应于DNA损伤和复制阻滞，细胞周期进程通过控制关键细胞周期调节剂而停止。该基因编码的蛋白质是一个细胞周期检查点调节器和假定的肿瘤抑制子。它包含一个与叉头相关的蛋白相互作用域，它对DNA损伤应答的激活是必不可少的，并且对复制阻滞和DNA损伤应答被迅速磷酸化。当被激活时，已知编码蛋白抑制CDC25C磷酸酶，防止进入有丝分裂，并已显示稳定肿瘤抑制蛋白p53，导致细胞周期阻滞在G1。此外，这种蛋白质与磷酸化BRCA1相互作用，使BRCA1恢复DNA损伤后的存活。该基因的突变与Li-Fraumeni综合征有关，Li-Fraumeni综合征是一种高度渗透性的家族性癌症表型，通常与TP53的遗传突变有关。而且，这种基因的突变被认为是导致肉瘤、乳腺癌和脑瘤的易感因素。这种核蛋白是丝氨酸/苏氨酸蛋白激酶的CDS1亚家族成员。已经发现了几种编码不同亚型的转录本变体。[由RefSeq，APR 2012提供]