Jarid1B (also known as KDM5B or PLU1) is in the family of JHDM genes. These are responsible for demethylation of tri- and di-methylated lysines in the 4 position of histone 3 (H3K4me3 and H3K4me2). Jarid1B is a multidomain enzyme that is part of the subfamily KDM5.

JARID1B was implicated in repair of double strand breaks after its loss was shown to promote spontaneous DNA damage and sensitize both osteosarcoma and breast cancer cell lines to genotoxic insult. Here JARID1B was enriched at DNA damage sites, where it was required for recruiting Ku70 and BRCA1 during non-homologous end joining .

2020年10月27日 · CDX2 inhibited by JARID1B-derived H3K4me3 methylation promoted cells proliferation of CRC via Wnt/β-catenin signaling pathway. Therefore, our studies provided a novel insight into the role of JARID1B in CRC cells proliferation and …

2017年10月1日 · JARID1A, JARID1B, and JARID1C have been shown to promote EMT along with invasion and metastasis. JARID1B’s augmentation of PI3K–Akt signaling in hepatocellular carcinoma cells indirectly connects it to the EMT-promoting effects that occur downstream of …

2020年10月27日 · Jumonji AT-rich interactive domain 1B (JARID1B) has been shown to be upregulated in many human cancers and plays a critical role in the development of cancers cells. Nevertheless, its functional role in colorectal cancer (CRC) progression is not fully understood.

We identified the H3K4-demethylase Jarid1b as novel component of the Rb pathway in this screening model. We find that depletion of Jarid1b phenocopies knockdown of Rb1 and that Jarid1b associates with E2f-target genes during cellular senescence. These results suggest a role for Jarid1b in Rb-mediated repression of cell cycle genes during ...

Down-regulation of expression of JARID1B using shRNAi in MCF-7 cells resulted in a dramatic decrease in E2 stimulated tumour growth in nude mice. The data demonstrate a specific role for Jarid1B in early embryonic development, in the development and differentiation of the normal mammary gland, and in estrogen induced growth of ER+ breast cancer.

Here, we show that the H3K4me2/3 histone demethylase Jarid1b (Kdm5b/Plu1) is dispensable for ESC self-renewal, but essential for ESC differentiation along the neural lineage.

PLU-1 (also known as JARID1B or KDM5B) is highly expressed in 90% of ductal breast carcinomas and associated to the malignant phenotype of breast and prostate cancer [145–147]. Knockdown of JARID1B/PLU-1 expression results in reduced proliferation of MCF-7 breast carcinoma cells and in derepression of cellular genes like BRCA1 and HoxA5 [148].

JARID1B, a transcriptional repressor, targets genes involved in diverse cellular processes including development, differentiation, and cell cycle (21–23). It is overexpressed in various cancers (23–25). In OSCC, JARID1B silencing is observed to attenuate sphere formation and stem cell marker expression .