• Target：
• p27

• Fields：
• >>Endocrine resistance;>>ErbB signaling pathway;>>HIF-1 signaling pathway;>>FoxO signaling pathway;>>Cell cycle;>>PI3K-Akt signaling pathway;>>AGE-RAGE signaling pathway in diabetic complications;>>Cushing syndrome;>>Measles;>>Human papillomavirus infection;>>Epstein-Barr virus infection;>>Pathways in cancer;>>Transcriptional misregulation in cancer;>>Viral carcinogenesis;>>MicroRNAs in cancer;>>Prostate cancer;>>Chronic myeloid leukemia;>>Small cell lung cancer;>>Gastric cancer

• Gene Name：
• CDKN1B

• Protein Name：
• Cyclin-dependent kinase inhibitor 1B

• Human Gene Id：
• 1027

• Human Swiss Prot No：
• P46527

• Mouse Swiss Prot No：
• P46414

• Immunogen：
• Purified recombinant fragment of human p27 expressed in E. Coli.

• Specificity：
• p27 Monoclonal Antibody detects endogenous levels of p27 protein.

• Formulation：
• Liquid in PBS containing 50% glycerol, 0.5% BSA and 0.02% sodium azide.

• Source：
• Monoclonal, Mouse

• Dilution：
• WB 1:500 - 1:2000. ELISA: 1:10000. Not yet tested in other applications.

• Purification：
• Affinity purification

• Storage Stability：
• -15°C to -25°C/1 year(Do not lower than -25°C)

• Other Name：
• CDKN1B;KIP1;Cyclin-dependent kinase inhibitor 1B;Cyclin-dependent kinase inhibitor p27;p27Kip1

• Molecular Weight(Da)：
• 22kD

• References：
• 1. Exp Mol Med. 2009 Nov 30;41(11):765-71.
  2. Int J Gynecol Pathol. 2010 Jan;29(1):8-18.

• 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). [provided by RefSeq, Apr 2014],

• Function：
• disease:Defects in CDKN1B are the cause of multiple endocrine neoplasia type 4 (MEN4) [MIM:610755]. Multiple endocrine neoplasia (MEN) syndromes are inherited cancer syndromes of the thyroid. MEN4 is a MEN-like syndrome with a phenotypic overlap of both MEN1 and MEN2.,domain:A peptide sequence containing only AA 28-79 retains substantial Kip1 cyclin A/CDK2 inhibitory activity.,function:Important regulator of cell cycle progrssion. Involved in G1 arrest. Potent inhibitor of cyclin E- and cyclin A-CDK2 complexes. Positive regulator of cyclin D-dependent kinases such as CDK4. Regulated by phosphorylation and degradation events.,induction:Maximal levels in quiescence cells and early G(1). Levels decrease after mitogen stimulation as cells progress toward S-phase.,miscellaneous:Decreased levels of p27Kip1, mainly due to proteosomal degradation, are found in various epithelial tumors originati

• Subcellular Location：
• 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; this leads to lysosomal degradation (By similarity). .

• Expression：
• Expressed in kidney (at protein level) (PubMed:15509543). Expressed in all tissues tested (PubMed:8033212). Highest levels in skeletal muscle, lowest in liver and kidney (PubMed:8033212).

Long non‑coding RNA ENST00000547547 inhibits cell proliferation, invasion and migration in colorectal cancer cells. ONCOLOGY REPORTS Oncol Rep. 2019 Jan;41(1):483-491 WB Human 1:200 HCT116 cell, LoVo cell

Ai, Xiaohui, et al. "Long non-coding RNA ENST00000547547 inhibits cell proliferation, invasion and migration in colorectal cancer cells." Oncology reports 41.1 (2019): 483-491.

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