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>   首页   >   产品   >   一抗   >   精选抗体   >   P21CIP1(T57) Antibody   

P21CIP1(T57) Antibody

Purified Rabbit Polyclonal Antibody (Pab)

     
  • 1 - P21CIP1(T57) Antibody AP22485a
    All lanes: Anti-P21CIP1(T57) Antibody at 1:1000 dilution + Hela whole cell lysate Lysates/proteins at 20 µg per lane. Secondary: Goat Anti-Rabbit IgG, (H+L), Peroxidase conjugated (ASP1615) at 1/15000 dilution. Observed band size: 22 KDa Blocking/Dilution buffer: 5% NFDM/TBST.
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Product Information
Application
  • Applications Legend:
  • E=ELISA
  • WB=Western Blotting
  • IHC=Immunohistochemistry
  • IHC-P=Immunohistochemistry (Paraffin)
  • IP=Immunoprecipitation
  • IF=Immunofluorescence
  • IC=Immunochemistry
  • ICC=Immunocytochemistry
  • FC=Flow Cytometry
  • DB=Dot Blot
WB, E
Primary Accession P38936
Host Rabbit
Clonality polyclonal
Isotype Rabbit Ig
Calculated MW 18119 Da
Additional Information
Gene ID 1026
Other Names Cyclin-dependent kinase inhibitor 1, CDK-interacting protein 1, Melanoma differentiation-associated protein 6, MDA-6, p21, CDKN1A (HGNC:1784)
Target/Specificity This P21CIP1(T57) antibody is generated from a rabbit immunized with a KLH conjugated synthetic peptide between amino acids from the human region of human P21CIP1(T57).
Dilution WB~~1:1000
E~~Use at an assay dependent concentration.
Format Purified polyclonal antibody supplied in PBS with 0.05% (V/V) Proclin 300. This antibody is purified through a protein A column, followed by peptide affinity purification.
StorageMaintain refrigerated at 2-8°C for up to 2 weeks. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles.
PrecautionsP21CIP1(T57) Antibody is for research use only and not for use in diagnostic or therapeutic procedures.
Protein Information
Name CDKN1A (HGNC:1784)
Function Plays an important role in controlling cell cycle progression and DNA damage-induced G2 arrest (PubMed:9106657). Involved in p53/TP53 mediated inhibition of cellular proliferation in response to DNA damage. Also involved in p53-independent DNA damage-induced G2 arrest mediated by CREB3L1 in astrocytes and osteoblasts (By similarity). 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. Inhibits DNA synthesis by DNA polymerase delta by competing with POLD3 for PCNA binding (PubMed:11595739). Negatively regulates the CDK4- and CDK6-driven phosphorylation of RB1 in keratinocytes, thereby resulting in the release of E2F1 and subsequent transcription of E2F1-driven G1/S phase promoting genes (By similarity).
Cellular Location Cytoplasm. Nucleus
Tissue Location Expressed in all adult tissues, with 5-fold lower levels observed in the brain
Research Areas

For Research Use Only. Not For Use In Diagnostic Procedures.

BACKGROUND

Plays an important role in controlling cell cycle progression and DNA damage-induced G2 arrest (PubMed:9106657). Involved in p53/TP53 mediated inhibition of cellular proliferation in response to DNA damage. Also involved in p53-independent DNA damage-induced G2 arrest mediated by CREB3L1 in astrocytes and osteoblasts (By similarity). 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. Inhibits DNA synthesis by DNA polymerase delta by competing with POLD3 for PCNA binding (PubMed:11595739). Negatively regulates the CDK4- and CDK6-driven phosphorylation of RB1 in keratinocytes, thereby resulting in the release of E2F1 and subsequent transcription of E2F1-driven G1/S phase promoting genes (By similarity).

REFERENCES

Harper J.W.,et al.Cell 75:805-816(1993).
El-Deiry W.S.,et al.Cell 75:817-825(1993).
Xiong Y.,et al.Nature 366:701-704(1993).
Jiang H.,et al.Mol. Cell. Differ. 1:285-299(1993).
Jiang H.,et al.Oncogene 10:1855-1864(1995).

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