FITC标记的磷酸化p21蛋白抗体
产品名称： FITC标记的磷酸化p21蛋白抗体
英文名称： Anti-phospho-CDKN1A/p21 (Thr57)/FITC
产品编号： HZ-5238R-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： IF=1:50-200
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Rabbit Anti-phospho-CDKN1A/p21 (Thr57)/FITC Conjugated antibody
FITC标记的磷酸化p21蛋白抗体
| 英文名称 | Anti-phospho-CDKN1A/p21 (Thr57)/FITC |
| 中文名称 | FITC标记的磷酸化p21蛋白抗体 |
| 别 名 | CDKN1A/p21 (phospho Thr57); p21 (phospho T57); p21 (phospho Thr57); Activating Fragment 1; CAP20; Cation chloride cotransporter-interacting protein 1; CDK Interacting Protein 1; CDK-interacting protein 1; CDKI; CDKN 1; CDKN1; CDKN1A; CIP1; Cyclin Dependent Kinase Inhibitor 1A; Cyclin-dependent kinase inhibitor 1; Cyclin-dependent kinase inhibitor 1A (P21); Cyclin-dependent kinase inhibitor 1A (p21, Cip1); DNA Synthesis Inhibitor; MDA 6; MDA-6; MDA6; Melanoma Differentiation Associated Protein 6; Melanoma differentiation-associated protein 6; Melanoma differentiation-associated protein; p21; P21 protein; p21CIP1; p21WAF; PIC1; SDI1; SLC12A9; WAF1; Wildtype p53 Activating Fragment 1; Wildtype p53-activated fragment 1; CDN1A_HUMAN. |
| 规格价格 | 100ul/2980元 购买 大包装/询价 |
| 说 明 书 | 100ul |
| 产品类型 | 磷酸化抗体 |
| 研究领域 | 肿瘤 免疫学 信号转导 细胞周期蛋白 |
| 抗体来源 | Rabbit |
| 克隆类型 | Polyclonal |
| 交叉反应 | Human, Mouse, Rat, |
| 产品应用 | IF=1:50-200 not yet tested in other applications. optimal dilutions/concentrations should be determined by the end user. |
| 分 子 量 | 18kDa |
| 性 状 | Lyophilized or Liquid |
| 浓 度 | 1mg/ml |
| 免 疫 原 | KLH conjugated Synthesised phosphopeptide derived from human CDKN1A around the phosphorylation site of Thr57 [TE(p-T)PL] |
| 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: This gene encodes a potent cyclin-dependent kinase inhibitor. The encoded protein binds to and inhibits the activity of cyclin-CDK2 or -CDK4 complexes, and thus functions as a regulator of cell cycle progression at G1. The expression of this gene is tightly controlled by the tumor suppressor protein p53, through which this protein mediates the p53-dependent cell cycle G1 phase arrest in response to a variety of stress stimuli. This protein can interact with proliferating cell nuclear antigen (PCNA), a DNA polymerase accessory factor, and plays a regulatory role in S phase DNA replication and DNA damage repair. This protein was reported to be specifically cleaved by CASP3-like caspases, which thus leads to a dramatic activation of CDK2, and may be instrumental in the execution of apoptosis following caspase activation. Two alternatively spliced variants, which encode an identical protein, have been reported. Function: May be the important intermediate by which p53/TP53 mediates its role as an inhibitor of cellular proliferation in response to DNA damage. Binds to and inhibits cyclin-dependent kinase activity, preventing phosphorylation of critical cyclin-dependent kinase substrates and blocking cell cycle progression. Functions in the nuclear localization and assembly of cyclin D-CDK4 complex and promotes its kinase activity towards RB1. At higher stoichiometric ratios, inhibits the kinase activity of the cyclin D-CDK4 complex. Subunit: Interacts with HDAC1; the interaction is prevented by competitive binding of C10orf90/FATS to HDAC1 facilitating acetylation and protein stabilization of CDKN1A/p21. Interacts with MKRN1. Interacts with PSMA3. Interacts with PCNA. Component of the ternary complex, cyclin D-CDK4-CDKN1A. Interacts (via its N-terminal domain) with CDK4; the interaction promotes the assembly of the cyclin D-CDK4 complex, its nuclear translocation and promotes the cyclin D-dependent enzyme activity of CDK4. Binding to CDK2 leads to CDK2/cyclin E inactivation at the G1-S phase DNA damage checkpoint, thereby arresting cells at the G1-S transition during DNA repair. Interacts with PIM1. Subcellular Location: Cytoplasmic and Nuclear. Tissue Specificity: Expressed in spleen, liver and lung. Not detected in kidney, colon, stomach or brain. Post-translational modifications: Phosphorylation of Thr-145 by Akt or of Ser-146 by PKC impairs binding to PCNA. Phosphorylation at Ser-114 by GSK3-beta enhances ubiquitination by the DCX(DTL) complex. Phosphorylation of Thr-145 by PIM2 enhances CDKN1A stability and inhibits cell proliferation. Phosphorylation of Thr-145 by PIM1 results in the relocation of CDKN1A to the cytoplasm and enhanced CDKN1A protein stability. Ubiquitinated by MKRN1; leading to polyubiquitination and 26S proteasome-dependent degradation. Ubiquitinated by the DCX(DTL) complex, also named CRL4(CDT2) complex, leading to its degradation during S phase or following UV irradiation. Ubiquitination by the DCX(DTL) complex is essential to control replication licensing and is PCNA-dependent: interacts with PCNA via its PIP-box, while the presence of the containing the 'K+4' motif in the PIP box, recruit the DCX(DTL) complex, leading to its degradation. Acetylation leads to protein stability. Acetylated in vitro on Lys-141, Lys-154, Lys-161 and Lys-163. Deacetylation by HDAC1 is prevented by competitive binding of C10orf90/FATS to HDAC1. Similarity: Belongs to the CDI family. Database links: Entrez Gene: 1026 Human Entrez Gene: 12575 Mouse Entrez Gene: 114851 Rat Omim: 116899 Human SwissProt: P38936 Human SwissProt: P39689 Mouse Unigene: 370771 Human Unigene: 195663 Mouse Unigene: 10089 Rat Important Note: This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications. p21蛋白的过度表达与肿瘤的类型、恶性度、分期以及病人的预后密切相关。主要用于胃肠道癌肿、乳腺癌、肺癌等恶性肿瘤的研究 |
该基因编码一种强有力的细胞周期蛋白依赖性激酶抑制剂。编码的蛋白质结合并抑制细胞周期蛋白CDK2或-CDK4复合物的活性，从而起到调节G1期细胞周期进程的作用。该基因的表达由肿瘤抑制蛋白p53严格控制，通过该蛋白介导p53依赖的细胞周期G1期阻滞响应于各种应激刺激。这种蛋白可与增殖细胞核抗原（PCNA）、DNA聚合酶辅助因子相互作用，并在S期DNA复制和DNA损伤修复中起调节作用。据报道，这种蛋白被Casp3样的半胱氨酸天冬氨酸蛋白酶特异性裂解，从而导致CDK2的显著激活，并且可能在caspase活化后的细胞凋亡的执行中起作用。两个交替剪接变异体，编码相同的蛋白质，已报道。