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DNA-binding protein involved in S phase checkpoint control-coupled apoptosis by mediating p53/TP53-induced apoptosis. Additionally we are shipping and many more products for this protein.
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Human Polyclonal KLLN Primary Antibody for WB - ABIN655558
Cho, Liang: Killin is a p53-regulated nuclear inhibitor of DNA synthesis. in Proceedings of the National Academy of Sciences of the United States of America 2008
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The results suggest a critical role for KLLN as a potential regulator of pericentric heterochromatin formation, genomic stability and gene expression.
overexpression of microRNA-224 enhanced the proliferation abilities of HO8910 and knockdown of microRNA-224 suppressed the proliferation abilities of HO8910PM by KLLN-cyclin A (show CCNA2 Antibodies) pathway.
Germline promoter hypermethylation of KLLN is associated with particular malignant and benign Cowden syndrome features, which is dependent on the PTEN (show PTEN Antibodies) mutation status.
Killin has a role in competitively inhibiting the formation of DNA replication forks during S-phase, as well as potentially negatively regulate RNA synthesis during other cell cycle phases
Data indicate that NVP-BEZ235-induced androgen receptor (AR (show AR Antibodies)) suppression resulted in decreased expression of both tumor suppressor proteins PTEN (show PTEN Antibodies) and KLLN in AR+/ER+ breast cancer cells.
Nuclear KLLN expression associates with improved relapse-free survival for prostate carcinoma
We demonstrate, in vitro and in murine xenograph models, that both KLLN and PTEN (show PTEN Antibodies) are AR-target genes, mediating androgen-induced growth inhibition and apoptosis in breast cancer cells.
Germline KLLN mutations dysregulate the cell cycle at G2.
KLLN is a transcription factor directly regulating AR, TP53 (show TP53 Antibodies), and TP73 (show TP73 Antibodies) expression, with a role in prostate carcinogenesis.
Pathogenic mutations in KLLN are rare in breast cancer families and the c.339_340delAG variant does not represent a high-penetrance breast cancer risk allele.
DNA-binding protein involved in S phase checkpoint control-coupled apoptosis by mediating p53/TP53-induced apoptosis. Has the ability to inhibit DNA synthesis and S phase arrest coupled to apoptosis. Has affinity to both double- and single- stranded DNA.