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For research use only.

Verified Samples Verified Samples in IHC: Human lung cancer, Human liver cancer, Rat spleen cancer, Human prostate
Dilution IHC 1:100-1:400
Isotype IgG
Host Rabbit
Reactivity Human,  Rat
Applications IHC
Clonality Polyclonal
Immunogen KLH conjugated Synthetic peptide corresponding to Mouse P27 KIP1
Abbre p27
Synonyms AA408329,  AI843786,  CDKN 1B,  CDKN 4,  CDKN1B,  CDKN4,  CDN1B,  Cdki1b,  Cyclin Dependent Kinase Inhibitor 1B,  Cyclin dependent kinase inhibitor p27,  Cyclin-dependent kinase inhibitor 1B,  Cyclin-dependent kinase inhibitor 1B (p27,  Cyclin-dependent kinase inhibitor p2,  Kip1)
Swissprot
Cellular Localization Nucleus. Cytoplasm. Endosome. Nuclear and cytoplasmic in quiescent cells. AKT-or RSK-mediated phosphorylation on Thr-198, binds 14-3-3, translocates to the cytoplasm and promotes cell cycle progression. Mitogen-activated UHMK1 phosphorylation on Ser-10 also results in translocation to the cytoplasm and cell cycle progression. Phosphorylation on Ser-10 facilitates nuclear export. Translocates to the nucleus on phosphorylation of Tyr-88 and Tyr-89. Colocalizes at the endosome with SNX6 and this leads to lysosomal degradation.
Concentration 0.89 mg/mL
Buffer Phosphate buffered solution, pH 7.4, containing 0.05% stabilizer, 1% protein protectant and 50% glycerol.
Purification Method Affinity purification
Research Areas Cancer,  Cell Biology,  Epigenetics and Nuclear Signaling
Conjugation Unconjugated
Storage Store at -20°C Valid for 12 months. Avoid freeze / thaw cycles.
Shipping The product is shipped with ice pack,upon receipt,store it immediately at the temperature recommended.
background This gene encodes a cyclin-dependent kinase inhibitor, which shares a limited similarity with CDK inhibitor CDKN1A/p21. The encoded protein binds to and prevents the activation of cyclin E-CDK2 or cyclin D-CDK4 complexes, and thus controls the cell cycle progression at G1. The degradation of this protein, which is triggered by its CDK dependent phosphorylation and subsequent ubiquitination by SCF complexes, is required for the cellular transition from quiescence to the proliferative state. Mutations in this gene are associated with multiple endocrine neoplasia type IV (MEN4).
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Unconjugated

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