本公司经销phospho-CDKN1A/P21 （Ser146），磷酸化p21蛋白抗体，克隆类型为polyclonal，宿主来源是Rabbit，phospho-CDKN1A/P21 （Ser146）磷酸化p21蛋白抗体可应用于WB、elisa、IP、IF、IHC等实验，欢迎垂询订购！

货号：BY-5239R
英文名称：Anti-phospho-CDKN1A/P21 （Ser146）
中文名称：磷酸化p21蛋白抗体
其他名称：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.
抗体来源：Rabbit
克隆类型：polyclonal
蛋白分子量：predicted molecular weight: 18kDa
纯化方法：affinity purified by Protein A
交叉反应：hu, dog, cow, shp, pig, Gpig
产品介绍：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. Two families of cyclin dependent kinase inhibitors （CKIs） have been identified. The p21WAF1/Cip1 family inhibits all kinases involved in the G1/S transition. The p16INK4a family inhibits Cdk4 ａnd Cdk6 specifically.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 : Cytoplasm. Nucleus.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 : UniProtKB/Swiss-Prot: P38936.3p21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。