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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 16

The reciprocal translocation t(1;3)(p36;q21) occurs in a subset of myelodysplastic syndrome (MDS) and acute myeloid leukemia (AML). This gene is located near the 1p36.3 breakpoint and has been shown to be specifically expressed in the t(1:3)(p36,q21)-positive MDS/AML. The protein encoded by this gene is a zinc finger transcription factor and contains an N-terminal PR domain. The translocation results in the overexpression of a truncated version of this protein that lacks the PR domain, which may play an important role in the pathogenesis of MDS and AML. Alternatively spliced transcript variants encoding distinct isoforms have been reported. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: UCP1, Mel, CAN, BAT, HAD
Papers on MEL-1
Mitofusin 2 maintains haematopoietic stem cells with extensive lymphoid potential.
Snoeck et al., New York City, United States. In Nature, Feb 2016
Here we show in mice that the short isoform of a critical regulator of HSCs, Prdm16 (refs 4, 5), induces mitofusin 2 (Mfn2), a protein involved in mitochondrial fusion and in tethering of mitochondria to the endoplasmic reticulum.
Intermedin/Adrenomedullin 2 polypeptide promotes adipose tissue browning and reduces high-fat diet-induced obesity and insulin resistance in mice.
Wang et al., Beijing, China. In Int J Obes (lond), Feb 2016
These effects may be due to increased AMP-activated protein kinase (AMPK) phosphorylation and reduced peroxisome proliferator-activated receptor gamma co-activator 1α (PGC1α) acetylation, which result in interactions between PGC1α and PR domain containing 16 (PRDM16) and then promote uncoupling protein 1 (UCP1) expression in adipocytes.
Dysfunctional subcutaneous fat with reduced Dicer and brown adipose tissue gene expression in HIV-infected patients.
Grinspoon et al., Bethesda, United States. In J Clin Endocrinol Metab, Feb 2016
Dicer expression was decreased in abdominal SC fat of HIV vs. non-HIV (4.88 [1.91, 11.93] vs.17.69 [10.72, 47.91], P=0.01), as were PGC1α, ZIC1, PRDM16, DIO2, and HSP60 (all P≤0.03).
Pre-Meiotic Anther Development: Cell Fate Specification and Differentiation.
Egger et al., Stanford, United States. In Annu Rev Plant Biol, Feb 2016
Here we describe the modern interpretation of pre-meiotic anther development, from the earliest cell specifications within the anther lobes through SPL/NZZ-, MSP1-, and MEL1-dependent pathways as well as the initial setup of the abaxial and adaxial axes and outgrowth of the anther lobes.
Cell-Autonomous Brown-Like Adipogenesis of Preadipocytes from Retinoblastoma Haploinsufficient Mice.
Ribot et al., Palma, Spain. In J Cell Physiol, Feb 2016
Primary white Rb(+/-) adipocytes displayed under basal conditions increased glucose uptake and an enhanced expression of brown adipocyte-related genes (Pparg, Ppargc1a, Ppargc1b, Prdm16, Cpt1b), but not of purported beige/brite transcriptional markers (Cd137, Tmem26, Tbx1, Slc27a1, Hoxc9, Shox2).
The Multifaceted Roles of PRDM16: Adipose Biology and Beyond.
Cohen et al., New York City, United States. In Trends Endocrinol Metab, Jan 2016
Studies have indicated crucial roles for PRDM16 in the determination and function of brown and beige fat as well as in hematopoiesis and cardiac development, highlighting the importance of PRDM16 in developmental processes in different tissues.
miR-101 reverses hypomethylation of the PRDM16 promoter to disrupt mitochondrial function in astrocytoma cells.
Wu et al., Changsha, China. In Oncotarget, Jan 2016
UNASSIGNED: Our previous report identified PR domain containing 16 (PRDM16), a member of the PR-domain gene family, as a new methylation associated gene in astrocytoma cells.
Identification of genomic aberrations in hemangioblastoma by droplet digital PCR and SNP microarray highlights novel candidate genes and pathways for pathogenesis.
Toren et al., Tel Aviv-Yafo, Israel. In Bmc Genomics, Dec 2015
These regions contain the EGFR and PRDM16 genes.
1p36 deletion syndrome: an update.
Scott et al., Houston, United States. In Appl Clin Genet, 2014
In particular, we highlight evidence implicating MMP23B, GABRD, SKI, PRDM16, KCNAB2, RERE, UBE4B, CASZ1, PDPN, SPEN, ECE1, HSPG2, and LUZP1 in various 1p36 deletion phenotypes.
Shades of brown: a model for thermogenic fat.
Sul et al., Berkeley, United States. In Front Endocrinol (lausanne), 2014
Here, we highlight recent advances in the understanding of brown and beige/brite adipocytes as well as transcriptional regulation for development and function of murine brown and beige/brite adipocytes focusing on EBF2, IRF4, and ZFP516, in addition to PRDM16 as a coregulator.
Control of adipocyte differentiation in different fat depots; implications for pathophysiology or therapy.
James et al., Sydney, Australia. In Front Endocrinol (lausanne), 2014
Basic control of differentiation is similar in BAT but important differences include the effect of PGC-1α on mitochondrial biosynthesis and upregulation of UCP1; also PRDM16 plays a pivotal role in expression of the BAT phenotype.
Brown adipose tissue activity as a target for the treatment of obesity/insulin resistance.
Rohner-Jeanrenaud et al., Genève, Switzerland. In Front Physiol, 2014
Interestingly, similar results were obtained by adipose tissue-specific overexpression of PR-domain-containing 16 (PRDM16) or BMP4 in mice.
Inhibition of Notch signaling promotes browning of white adipose tissue and ameliorates obesity.
Kuang et al., West Lafayette, United States. In Nat Med, 2014
At the molecular level, constitutive activation of Notch signaling inhibits, whereas Notch inhibition induces, Ppargc1a and Prdm16 transcription in white adipocytes.
IRF4 is a key thermogenic transcriptional partner of PGC-1α.
Rosen et al., Boston, United States. In Cell, 2014
IRF4 also induces the expression of PGC-1α and PRDM16 and interacts with PGC-1α, driving Ucp1 expression.
A smooth muscle-like origin for beige adipocytes.
Spiegelman et al., Boston, United States. In Cell Metab, 2014
Finally, ectopic expression of PRDM16 converts bona fide vascular smooth muscle cells into Ucp1-positive adipocytes in vitro.
Prdm3 and Prdm16 are H3K9me1 methyltransferases required for mammalian heterochromatin integrity.
Jenuwein et al., Freiburg, Germany. In Cell, 2012
Data identify Prdm3 and Prdm16 as H3K9me1 methyltransferases and expose a functional framework in which anchoring to the nuclear periphery helps maintain the integrity of mammalian heterochromatin.
Association of genetic variations of PRDM16 with metabolic syndrome in a general Xinjiang Uygur population.
Ling et al., In Endocrine, 2012
genetic association studies in a Chinese Xinjiang Uygur population: Studies suggest that commonly occurring SNP in PRDM16 (rs2236518) shows a significant negative association with metabolic syndrome in a multivariable logistic regression analysis.
Chromatin immunoprecipitation-promoter microarray identification of genes regulated by PRDM16 in murine embryonic palate mesenchymal cells.
Pisano et al., Louisville, United States. In Exp Biol Med (maywood), 2012
These results suggest that PRDM16 may play a role in differentiation of mesenchymal cells in the embryonic secondary palate that contribute to the anterior, bony palate and posterior, muscular palate.
PRDM16 (1p36) translocations define a distinct entity of myeloid malignancies with poor prognosis but may also occur in lymphoid malignancies.
Belgian Cytogenetic Group for Haematology and Oncology (BCG-HO) et al., Brussels, Belgium. In Br J Haematol, 2012
Survival data suggest that patients with AML/MDS and PRDM16 translocations have a poor prognosis despite a simple karyotype and a median age of 65 years.
Genetics of migraine in the age of genome-wide association studies.
Schürks, Essen, Germany. In J Headache Pain, 2012
genome-wide association studies have successfully identified four new genetic variants associated with migraine in the LRP1, TRPM8, and PRDM16 genes
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