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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 Proteins (5) and PRDM16 Kits (1) and many more products for this protein.
Showing 10 out of 68 products:
Human Polyclonal PRDM16 Primary Antibody for EIA, IHC (p) - ABIN500533
Seale, Bjork, Yang, Kajimura, Chin, Kuang, Scimè, Devarakonda, Conroe, Erdjument-Bromage, Tempst, Rudnicki, Beier, Spiegelman: PRDM16 controls a brown fat/skeletal muscle switch. in Nature 2008
Show all 4 references for ABIN500533
Human Polyclonal PRDM16 Primary Antibody for ELISA, ICC - ABIN4347210
Baskaran, Krishnan, Ren, Thyagarajan: Capsaicin induces browning of white adipose tissue and counters obesity by activating TRPV1 channel-dependent mechanisms. in British journal of pharmacology 2016
Human Polyclonal PRDM16 Primary Antibody for ELISA, WB - ABIN184809
Mochizuki, Shimizu, Nagasawa, Tanaka, Taniwaki, Yokota, Morishita: A novel gene, MEL1, mapped to 1p36.3 is highly homologous to the MDS1/EVI1 gene and is transcriptionally activated in t(1;3)(p36;q21)-positive leukemia cells. in Blood 2000
Prdm3 (show MECOM Antibodies) 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.
High PRDM16 expression is associated with astrocytoma.
Our results suggest that K568 SUMOylation of sPRDM16 plays an important role in the progression of acute myeloid leukemia (show BCL11A Antibodies).
Results show that PRDM16 overexpression was highly recurrent in de novo paediatric AML (show RUNX1 Antibodies) 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 Antibodies) and MEL1 are homolog genes whose transcriptional activations by chromosomal translocations have roles in Japanese pediatric acute myeloid leukemia (show BCL11A Antibodies)
Three novel loci were identified in East Asians with cardiac arrhythmias: rs2483280 (PRDM16 locus) and rs335206 (PRDM6 (show PRDM6 Antibodies) locus) were associated with QRS (show QARS Antibodies) duration; and rs17026156 (SLC8A1 (show SLC8A1 Antibodies) locus) correlated with PR interval.
Genetic analyses uncovered the importance of the PRDM16 gene in the regulation of lean body mass.
MED1 (show MED1 Antibodies) is required for optimal PRDM16-induced Ucp1 (show UCP1 Antibodies) expression
PRDM2 (show PRDM2 Antibodies), PRDM5 (show PRDM5 Antibodies), 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.
We further show that Cdkn1c (show CDKN1C Antibodies) is required for post-transcriptional accumulation of the brown fat determinant PR domain containing 16 (PRDM16) and that CDKN1C (show CDKN1C Antibodies) and PRDM16 co-localise to the nucleus of rare label-retaining cell within iBAT (show SLC10A2 Antibodies).
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 Antibodies) and PPARgamma (show PPARG Antibodies) promoters
PRDM16 deficiency in BAT (show BAAT Antibodies) reduces MED1 (show MBD4 Antibodies) binding at PRDM16 target sites and causes a fundamental change in chromatin architecture at key brown fat-selective genes
Prdm16 and Prdm3 (show MECOM Antibodies) control postnatal BAT (show BAAT Antibodies) identity and function.
Study reveals that Prdm16 expression is regulated through Gcn5 (show KAT2A Antibodies)/PCAF (show KAT2B Antibodies) during brown adipogenesis.
these studies define the transcriptional pathways involved in HOXB4 (show HOXB4 Antibodies) HSC (show FUT1 Antibodies) expansion in vivo and identify repression of Prdm16 transcription as a mechanism by which expanding HSCs avoid leukemic transformation.
miR (show MLXIP Antibodies)-133 links to energy balance through targeting Prdm16.
These findings indicate that PRDM16 and beige (show LYST Antibodies) 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 (show UTS2R Antibodies) 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