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The reciprocal translocation t(1\;3)(p36\;q21) occurs in a subset of myelodysplastic syndrome (MDS) and acute myeloid leukemia (AML). Additionally we are shipping PRDM16 Antibodies (65) and PRDM16 Kits (1) and many more products for this protein.
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Prdm3 (show MECOM Proteins) and prdm16 are strongly expressed in the pharyngeal arches during cranioskeletal development, and their knockdown leads to defects in both the viscerocranium and the neurocranium.
Animals with the homozygote PRDM16 genotype had lower body weight and average daily gain than those with the other genotypes.
The genetic variation within PRDM16 gene in 1031 Chinese indigenous bovine, was analyzed.
Our results suggest that K568 SUMOylation of sPRDM16 plays an important role in the progression of acute myeloid leukemia (show BCL11A Proteins).
Results show that PRDM16 overexpression was highly recurrent in de novo paediatric AML (show RUNX1 Proteins) and is associated with adverse outcome
PRDM16 might contribute to maintain adipose tissue "white fat" gene expression profile and systemic metabolic homeostasis.
EVI1 (show MECOM Proteins) and MEL1 are homolog genes whose transcriptional activations by chromosomal translocations have roles in Japanese pediatric acute myeloid leukemia (show BCL11A Proteins)
Three novel loci were identified in East Asians with cardiac arrhythmias: rs2483280 (PRDM16 locus) and rs335206 (PRDM6 (show PRDM6 Proteins) locus) were associated with QRS (show QARS Proteins) duration; and rs17026156 (SLC8A1 (show SLC8A1 Proteins) locus) correlated with PR interval.
Genetic analyses uncovered the importance of the PRDM16 gene in the regulation of lean body mass.
MED1 (show MED1 Proteins) is required for optimal PRDM16-induced Ucp1 (show UCP1 Proteins) expression
PRDM2 (show PRDM2 Proteins), PRDM5 (show PRDM5 Proteins), PRDM16 promoters are methylated and their expression is suppressed in lung cancer cells.
Mutations in gene encoding the transcriptional co-activator PRDM16 may be a cause of left-ventricular noncompaction and dilated cardiomyopathy.
The rs2651899 variant in PRDM16 plays a role in Chinese common migraine susceptibility.
We further show that Cdkn1c (show CDKN1C Proteins) is required for post-transcriptional accumulation of the brown fat determinant PR domain containing 16 (PRDM16) and that CDKN1C (show CDKN1C Proteins) and PRDM16 co-localise to the nucleus of rare label-retaining cell within iBAT (show SLC10A2 Proteins).
PRDM16-induced C2C12 transdifferentiation is associated with alterations in CpG methylation of myogenic factors, and PR domain affects both myogenesis and adipogenesis with modified histone methylation marks on MyoD (show MYOD1 Proteins) and PPARgamma (show PPARG Proteins) promoters
PRDM16 deficiency in BAT (show BAAT Proteins) reduces MED1 (show MBD4 Proteins) binding at PRDM16 target sites and causes a fundamental change in chromatin architecture at key brown fat-selective genes
Prdm16 and Prdm3 (show MECOM Proteins) control postnatal BAT (show BAAT Proteins) identity and function.
Study reveals that Prdm16 expression is regulated through Gcn5 (show KAT2A Proteins)/PCAF (show KAT2B Proteins) during brown adipogenesis.
these studies define the transcriptional pathways involved in HOXB4 (show HOXB4 Proteins) HSC (show FUT1 Proteins) expansion in vivo and identify repression of Prdm16 transcription as a mechanism by which expanding HSCs avoid leukemic transformation.
miR (show MLXIP Proteins)-133 links to energy balance through targeting Prdm16.
These findings indicate that PRDM16 and beige adipocytes are required for the "browning" of white fat and the healthful effects of subcutaneous adipose tissue.
adult satellite cells give rise to brown adipocytes and that microRNA-133 regulates the choice between myogenic and brown adipose determination by targeting the 3'UTR of Prdm16.
When expressed at elevated levels in brown fat, TLE3 counters Prdm16, suppressing brown-selective genes and inducing white-selective genes, resulting in impaired fatty acid oxidation and thermogenesis.
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.
PR domain containing 16
, PR domain zinc finger protein 16-like
, MDS1/EVI1-like gene 1
, PR domain zinc finger protein 16
, transcription factor MEL1
, PR domain-containing protein 16
, line 27