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PRDM14 encodes a member of the PRDI-BF1 and RIZ homology domain containing (PRDM) family of transcriptional regulators. Additionally we are shipping PRDM14 Antibodies (69) and many more products for this protein.
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the H3K27-specific demethylase Utx (show KDM6A Proteins) regulates the expression of the master regulators for XCI and XCR: Prdm14, Tsix, and Xist.
Both TET1 (show TET1 Proteins) and TET2 are required for the repression of embryonic stem cells differentiation by PRDM14.
Upregulation of Prdm14 results in a highly homogeneous population of authentic pluripotent colonies and prevents the abnormal silencing of the Dlk1 (show DLK1 Proteins)-Dio3 (show DIO3 Proteins) locus.
PRDM14 is heterogeneously expressed in 4-cell-stage embryos. Forced expression of PRDM14 at the 2-cell stage leads to increased H3R26me2 and can induce a pluripotent ICM fate.
PRDM14-induced leukemic cells contain high levels of activated NOTCH1 (show NOTCH1 Proteins) and downstream NOTCH1 (show NOTCH1 Proteins) targets, including MYC (show MYC Proteins) and HES1, and are sensitive to pharmacological inhibition of NOTCH1 (show NOTCH1 Proteins) with the gamma-secretase inhibitor DAPT
PRDM14 physically interacts with TET1 (show TET1 Proteins) and TET2 and enhances the recruitment of TET1 (show TET1 Proteins) and TET2 at target loci. Knockdown of TET1 (show TET1 Proteins) and TET2 impaired transcriptional regulation and DNA demethylation by PRDM14.
Tsix and PRDM14 directly link X-chromosome reactivation to stem cell pluripotency.
Prdm14 promotes germline fate and naive pluripotency by repressing FGF signalling and DNA methylation (show HELLS Proteins).
PRDM14, ensures naive pluripotency through antagonizing activation of the FGFR (show FGFR2 Proteins) signaling by the core pluripotency transcriptional circuitry, and repressing expression of DNA methyltransferases that modify the epigenome to a primed epiblast-like state.
data provide the first direct evidence for the association of Prdm14 with cancer initiation in an in vivo mouse model and in human lymphoid malignancies, while suggesting mechanisms for Prdm14's mode of action
Prdm14 regulates Caudal primary axon outgrowth through activation of islet2 expression.
In response to cytokines, pluripotent stem cells differentiate first into a heterogeneous mesoderm-like cell population and then into Primordial Germ cell-Like Cells, which exhibit minimal PRDM14 expression.
The contribution of methylation-mediated gene silencing of PRDM14 to apoptosis evasion in HPV-positive cancer cells offers novel therapeutic options for HPV-induced cancers.
PRDM14 associated with cell differentiation in NSCLC.
Study reveals a repressive role of PRDM14 in the maintenance and induction of pluripotency and identifies PRDM14 as a new regulator of PRC2.
The high expression of PRDM14 in non-small cell lung cancer is associated with differentiation and histological type.
novel hESC regulators wherein PRDM14 exemplifies a key transcription factor required for the maintenance of hESC identity and the reacquisition of pluripotency in human somatic cells
PRDM14 mRNA is overexpressed in about two thirds of breast cancers; moreover, immunohistochemical analysis showed that expression of PRDM14 protein is also up-regulated.
These results suggest that PRDM14 is involved in the maintenance of the self-renewal of human ES cells by suppression of gene expression.
This gene encodes a member of the PRDI-BF1 and RIZ homology domain containing (PRDM) family of transcriptional regulators. The encoded protein may possess histone methyltransferase activity and plays a critical role in cell pluripotency by suppressing the expression of differentiation marker genes. Expression of this gene may play a role in breast cancer.
PR domain containing 14
, PR domain zinc finger protein 14
, PR domain-containing protein 14
, PR domain zinc finger protein 14-like