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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Dec 2016.

PR domain containing 5

PRDM5, PfM2, PR domain containing 5 PFM2
The protein encoded by this gene is a transcription factor of the PR-domain protein family. It contains a PR-domain and multiple zinc finger motifs. Transcription factors of the PR-domain family are known to be involved in cell differentiation and tumorigenesis. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: RIZ1, HAD, Qin, Blimp-1, POLYMERASE
Papers on PRDM5
A role for repressive complexes and H3K9 di-methylation in PRDM5-associated brittle cornea syndrome.
Manson et al., Boston, United States. In Hum Mol Genet, Jan 2016
Type 2 brittle cornea syndrome (BCS2) is an inherited connective tissue disease with a devastating ocular phenotype caused by mutations in the transcription factor PR domain containing 5 (PRDM5) hypothesized to exert epigenetic effects through histone and DNA methylation.
Whole exome sequencing identifies a heterozygous missense variant in the PRDM5 gene in a family with Axenfeld-Rieger syndrome.
den Hollander et al., Nijmegen, Netherlands. In Neurogenetics, Nov 2015
A novel heterozygous PRDM5 missense variant (c.877A>G; p.Lys293Glu) was found to segregate with the disease in an autosomal dominant fashion.
Methylation and expression of the tumour suppressor, PRDM5, in colorectal cancer and polyp subgroups.
Whitehall et al., Brisbane, Australia. In Bmc Cancer, 2014
BACKGROUND: PRDM5 is an epigenetic regulator that has been recognized as an important tumour suppressor gene.
Bruch's membrane abnormalities in PRDM5-related brittle cornea syndrome.
Black et al., Valencia, Spain. In Orphanet J Rare Dis, 2014
Recessive mutations in transcription factors ZNF469 and PRDM5 cause BCS.
Brittle Cornea Syndrome: Case Report with Novel Mutation in the PRDM5 Gene and Review of the Literature.
Cursiefen et al., Köln, Germany. In Case Rep Ophthalmol Med, 2014
A novel mutation, the homozygous variant c.17T>G, p.V6G, was found in the gene for PR-domain-containing protein 5 (PRDM5) in exon 1. Brittle cornea syndrome is a rare connective tissue disease with typical ocular, auditory, musculoskeletal, and cutaneous disorders.
Enrichment of pathogenic alleles in the brittle cornea gene, ZNF469, in keratoconus.
Willoughby et al., Lausanne, Switzerland. In Hum Mol Genet, 2014
Homozygous mutations in ZNF469 and PR domain-containing protein 5 (PRDM5) genes result in brittle cornea syndrome (BCS) Types 1 and 2, respectively.
Prdm5 suppresses Apc(Min)-driven intestinal adenomas and regulates monoacylglycerol lipase expression.
Lund et al., Copenhagen, Denmark. In Oncogene, 2014
PRDM5 is a poorly characterized member of the PRDM family for which several studies have reported a high frequency of promoter hypermethylation in cancer types of gastrointestinal origin.
Promoter methylation-mediated downregulation of PRDM5 contributes to the development of lung squamous cell carcinoma.
Liu et al., Changsha, China. In Tumour Biol, 2014
PRDM5 has been proposed as a tumor suppressor frequently downregualted in tumor.
Methylation of PRDM2, PRDM5 and PRDM16 genes in lung cancer cells.
Liu et al., Changsha, China. In Int J Clin Exp Pathol, 2013
AIMS: To investigate the changes of expression and methylation status of PRDM2, PRDM5, PRDM16 in lung cancer cells after treatment with demethylation agent.
ZNF469 frequently mutated in the brittle cornea syndrome (BCS) is a single exon gene possibly regulating the expression of several extracellular matrix components.
Giunta et al., Zürich, Switzerland. In Mol Genet Metab, 2013
Brittle cornea syndrome (BCS; MIM 229200) is an autosomal recessive generalized connective tissue disorder caused by mutations in ZNF469 and PRDM5.
Redundant roles of PRDM family members in zebrafish craniofacial development.
Artinger et al., Aurora, United States. In Dev Dyn, 2013
prdm3 and prdm16 are strongly expressed in the pharyngeal arches, while prdm5 is expressed specifically in the area of the forming neurocranium.
Identification of a novel ZNF469 mutation in a large family with Ehlers-Danlos phenotype.
Alkuraya et al., Riyadh, Saudi Arabia. In Gene, 2013
BCS-1 and BCS-2 are caused by recessive mutations in ZNF469 and PRDM5, respectively.
Homozygosity mapping in an anophthalmic pedigree provides evidence of additional genetic heterogeneity.
Lehmann et al., Edmonton, Canada. In Ophthalmic Genet, 2012
No CNVs were identified that segregated with the disease phenotype, and sequencing of five candidate genes (PRDM5, FGF2, SOS2, POU2F2 and CIC) did not identify any mutations.
Brittle cornea syndrome: recognition, molecular diagnosis and management.
Black et al., Manchester, United Kingdom. In Orphanet J Rare Dis, 2012
Two genes, ZNF469 and PRDM5, have now been identified, in which causative pathogenic mutations collectively account for the condition in nearly all patients with BCS ascertained to date.
Prdm5 regulates collagen gene transcription by association with RNA polymerase II in developing bone.
Lund et al., Copenhagen, Denmark. In Plos Genet, 2011
PRDM5 has been reported to predominantly repress transcription, but a characterization of its molecular functions in a relevant biological context is lacking.
Mutations in PRDM5 in brittle cornea syndrome identify a pathway regulating extracellular matrix development and maintenance.
Black et al., Manchester, United Kingdom. In Am J Hum Genet, 2011
ZNF469 and PRDM5, two genes that when mutated cause brittle cornea syndrome, participate in the same regulatory pathway.
DNA methylation and carcinogenesis of PRDM5 in cervical cancer.
Lou et al., Harbin, China. In J Cancer Res Clin Oncol, 2010
Data show that reduced expression of PRDM5 may play an important role in the pathogenesis and/or development of cervical cancer, and is considered to be caused in part by aberrant DNA methylation.
The epigenetic modifier PRDM5 functions as a tumor suppressor through modulating WNT/β-catenin signaling and is frequently silenced in multiple tumors.
Tao et al., Hong Kong, Hong Kong. In Plos One, 2010
Frequent epigenetic silencing of PRDM5 is involved in multiple tumorigeneses, which could serve as a tumor biomarker
Epigenetic regulation of protein-coding and microRNA genes by the Gfi1-interacting tumor suppressor PRDM5.
Horwitz et al., Seattle, United States. In Mol Cell Biol, 2007
Results identify PRDM5, which acts as a sequence-specific, DNA binding transcription factor that targets hematopoiesis-associated protein-coding and microRNA genes, some of which are targets of Gfi1.
PRDM5 identified as a target of epigenetic silencing in colorectal and gastric cancer.
Tokino et al., Sapporo, Japan. In Clin Cancer Res, 2007
Data suggest that epigenetic alteration of PRDM5 (e.g., methylation of its 5'-CpG island or trimethylation of Lys(27) of histone H3) likely plays a key role in the progression of gastrointestinal cancers and may be a useful molecular marker.
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