蛋白

p21CIP1重组蛋白

MBS515251

0.02毫克

270美元

重组蛋白

p21CIP1重组蛋白

[p21CIP1]

[CDKN1A;P21;SDI1;WAF1;CAP20;CDKN1;MDA-6]

[Homo sapiens cyclin-dependent kinase inhibitor 1A (p21, Cip1) (CDKN1A), transcript variant 1, mRNA; Cyclin-dependent kinase inhibitor 1; cyclin-dependent kinase inhibitor 1; DNA synthesis inhibitor; CDK-interacting protein 1; CDK-interaction protein 1; wild-type p53-activated fragment 1; melanoma differentiation associated protein 6; cyclin-dependent kinase inhibitor 1A (p21, Cip1); CDK-interacting protein 1; Melanoma differentiation-associated protein 6; MDA-6; p21]

[p21CIP1]

[CDKN1A;P21;SDI1;WAF1;CAP20;CDKN1;MDA-6]

[CDKN1A;CDKN1A;P21;CIP1;SDI1;WAF1;CAP20;CDKN1;MDA-6;p21CIP1;CAP20;CDKN1;CIP1;MDA6;PIC1;SDI1;WAF1;MDA-6]

CDN1A_HUMAN

2175

>70%

50mM三羟甲基氨基甲烷氯化氢, pH值7.5, 150mM氯化钠, 10mM谷胱甘肽, 0.1mM乙二胺四乙酸, 0.25mM DTT, 0.1mM苯甲基磺酰氟, 25% 甘油

0.2微克/微升

Store product at -70°C. For optimal storage, aliquot target into smaller quantities after centrifugation and store at recommended temperature. For most favorable performance, avoid repeated handling and multiple freeze/thaw cycles. Shipping: Ships with dry ice

Kinase Assay, Western Blot (WB)

十二烷基磺酸钠-PAGE

Scientific Background: CIP 1 (Cyclin-Dependent Kinase Inhibitor 1A) regulates cell cycle progression, terminal differentiation, and apoptosis (1). CIP1 was shown to be induced by p53 and to be a potent inhibitor of cyclin-dependent kinase (CDK) activity. DNA damage leads to increased expression of CIP1 in cyclin E-containing complexes and to an associated decrease in cyclin-dependent kinase activity. CIP1 is a critical downstream effector in the p53-specific pathway of growth control in mammalian cells (2).

Expression System: E.coli. Species: Human

Cell Cycle Proteins; Signaling Proteins - Cell Cycle Proteins

Recombinant full-length human p21CIP1 was expressed in E. coli cells using a N-terminal GST tag. Scientific Background: CIP 1 (Cyclin-Dependent Kinase Inhibitor 1A) regulates cell cycle progression, terminal differentiation, and apoptosis (1). CIP1 was shown to be induced by p53 and to be a potent inhibitor of cyclin-dependent kinase (CDK) activity. DNA damage leads to increased expression of CIP1 in cyclin E-containing complexes and to an associated decrease in cyclin-dependent kinase activity. CIP1 is a critical downstream effector in the p53-specific pathway of growth control in mammalian cells (2).

1. el-Deiry, W S. et al: WAF1/CIP1 is induced in p53-mediated G1 arrest and apoptosis. Cancer Res. 1994;54(5):1169-74. 2. Wagner, M. et al: Cyclin-dependent kinase-inhibitor 1 (CDKN1A) in the squamous epithelium of the oropharynx: possible implications of molecular biology and compartmentation. Anticancer Res. 2001; 21(1A):333-45.

310832422

NP_000380.1

NM_000389

P38936

~46 kDa

AKT Phosphorylates Targets In The Cytosol Pathway (106475); AMPK Signaling Pathway (198868); Adaptive Immune System Pathway (366160); Adipogenesis Pathway (198832); AhR Pathway (755436); Alpha6-Beta4 Integrin Signaling Pathway (198807); Androgen Receptor Signaling Pathway (198806); Angiopoietin Receptor Tie2-mediated Signaling Pathway (137917); Bladder Cancer Pathway (83115); Bladder Cancer Pathway (527)

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. Multiple alternatively spliced variants have been found for this gene. [provided by RefSeq, Nov 2010]

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. Ref.1 Ref.13. Subunit structure: Interacts with HDAC1; the interaction is prevented by competitive binding of C10orf90/FATS to HDAC1 facilitating acetylation and protein stabilization of CDKN1A/p21 . By similarity. 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. Ref.13 Ref.14 Ref.16 Ref.19 Ref.21 Ref.23 Ref.24. Subcellular location: Cytoplasm. Nucleus Ref.13 Ref.15 Ref.16. Tissue specificity: Expressed in all adult tissues, with 5-fold lower levels observed in the brain. Induction: Activated by p53/TP53, mezerein (antileukemic compound) and IFNB1. Repressed by HDAC1. Ref.1 Ref.2. Domain: The PIP-box K+4 motif mediates both the interaction with PCNA and the recuitment of the DCX(DTL) complex: while the PIP-box interacts with PCNA, the presence of the K+4 submotif, recruits the DCX(DTL) complex, leading to its ubiquitination. Ref.19 Ref.21The C-terminal is required for nuclear localization of the cyclin D-CDK4 complex. Ref.19 Ref.21. Post-translational modification: 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. Ref.19 Ref.20 Ref.21 Ref.24 Ref.25Acetylation 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 . By similarity. Sequence similarities: Belongs to the CDI family. Sequence caution: The sequence AAB59559.1 differs from that shown. Reason: Erroneous initiation. Translation N-terminally shortened.The sequence AAB59560.1 differs from that shown. Reason: Erroneous initiation. Translation N-terminally shortened.

0.02毫克

270美元

0.05毫克

450