Human CDKN1B blocking peptide

Name: Human CDKN1B blocking peptide
SKU: CDBP1689
Rating: 5 (1 reviews)

Synthetic Human CDKN1B blocking peptide for Apuri, BL, ELISA

COA

SDS

Datasheet

Summary

Product Overview

Blocking/Immunizing peptide for anti-KIP1/CDKN1B (internal) antibody

Target

KIP1 / CDKN1B (internal)

Nature

Synthetic

Tag/Conjugate

Unconjugated

Application Notes

For in vitro research use only. Not intended for any diagnostic or therapeutic purpose. Not for human or animal consumption.

Format

Lyophilized powder

Preservative

None

Storage

Shipped at ambient temperature, store at -20°C.

Entrez Gene ID

1027

Antigen Description

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

Hsp70 protein binding; chaperone binding; cyclin-dependent protein serine/threonine kinase inhibitor activity; contributes_to cysteine-type endopeptidase activator activity involved in apoptotic process; protein binding; protein complex binding; protein p

Synonyms

CDKN1B; cyclin-dependent kinase inhibitor 1B (p27, Kip1); KIP1; MEN4; CDKN4; MEN1B; P27KIP1; cyclin-dependent kinase inhibitor 1B;

Citations

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Documents

pdf COA

pdf SDS

pdf Datasheet

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Customer Reviews

References

CDKN1B Mediates Apoptosis of Neuronal Cells and Inflammation Induced by Oxyhemoglobin via miR-502-5p After Subarachnoid Hemorrhage

JOURNAL OF MOLECULAR NEUROSCIENCE

Authors: Chen, Dong; Wang, Xianwei; Huang, Jiaming; Cui, Sifu; Zhang, Liqiang

Abstract

Subarachnoid hemorrhage is a common disease in the neural system, which causes high fatality rate. Therefore, it is necessary to figure out inner mechanisms of factors related to this disease. RT-qPCR was applied for measuring expressions of CDKN1B and miR-502-5p and other factors of apoptosis and inflammation. Cell viabilities were detected through CCK-8. Binding conditions between miR-502-5p and CDKN1B were detected through luciferase report assay. Western blot was used for measuring levels of proteins in PPAR gamma/NF-kappa B signaling pathway. Apoptosis and inflammation of HT22 cell line, a kind of nerve cell line, were enhanced and viabilities were suppressed by oxyhemoglobin. CDKN1B expressed lower in induced HT22 cell line and overexpressed CDKN1B could promote viabilities and suppress apoptosis as well as inflammation. MiR-502-5p was the target gene of CDKN1B and enhanced apoptosis and inflammation of cells in HT22 cell line. Furthermore, miR-502-5p reversed functions of CKDN1B in induced cells through regulating proteins in PPAR gamma/NF-kappa B signaling pathway. CDKN1B was the gene that could inhibit SAH caused by apoptosis in nerve cells and inflammation by sponging miR-502-5p and regulating factors in PPAR gamma/NF-kappa B signaling pathway, suggesting it could be a factor for protecting functions of nerve cells after SAH.

CDKN1B 109VG and CDKN2A (540CG & 580CT) polymorphisms and susceptibility to colorectal cancer: A case-control study of the Iranian population

GENE REPORTS

Authors: Gohari, Nazanin; Saadat, Iraj

Abstract

Background: One of the most important factors leading to tumorigenesis is abnormality in the cells proliferation, because of the irregularity in cell cycle progression. CDKN2A (p16) and CDKN1B (p27) are tumor suppressors and regulators of cell cycle at G1 and G1-S transition. Any disorders in activity or expression of these two tumor suppressors can cause cancer. Aims: In this study, we appraised the relationship between 3 polymorphisms: p27 109VG (rs2066827) in exon1 and p16 [540CG (rs11515), 580CT (rs3088440)] in 3'UTR with the risk of colorectal cancer susceptibility in Iranian population. Subjects and methods: This case-control study was carried out on 214 cases with CRC and 233 control subjects. For p27 109VG and p16 (540CG, 580CT) genotyping, PCR-RFLP technique was used. Results: Logistic regression analysis revealed that G allele of p16 540CG significantly decreased the risk of CRC (OR = 0.63, CI = 0.42- 0.95, P = 0.031), but subjects with TT genotype of 580CT are more likely to develop CRC (OR = 4.63, CI = 1.28-16.71, P = 0.019). There were no significant relationships with p27 109VG and haplotype of p16 (540CG, 580CT) with CRC risk in Iranian population. However, coincidence in VG genotype of p27 109VG and CC genotype of p16 540CG has significantly increased the susceptibility to colorectal cancer (OR = 2.02, CI = 1.02-3.98, P = 0.042). Conclusion: This study indicates that the p16 [540CG (rs11515), 580CT (rs3088440)] polymorphisms are associated with the risk of CRC in Iranian population.