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anti-Human PRDM16 Antibodies:
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Human Polyclonal PRDM16 Primary Antibody for ELISA - ABIN249627
Stanford, Middelbeek, Townsend, An, Nygaard, Hitchcox, Markan, Nakano, Hirshman, Tseng, Goodyear: Brown adipose tissue regulates glucose homeostasis and insulin sensitivity. in The Journal of clinical investigation 2013
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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
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Human Polyclonal PRDM16 Primary Antibody for ELISA - ABIN546907
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
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.
We found a statistically significant difference in migraineurs with control for PRDM16 rs2651899 polymorphism at genotypic (p < 0.05), allelic (p = 0.022; OR 1.462; 95% CI 1.058-2.022) and for dominant model (p = 0.011; OR 1.957; 95% CI 1.169-3.276).
The rs2236518 at PRDM16 gene, maternal smoking, maternal passive smoking, and maternal drinking were closely related to the occurrence of nonsyndromic cleft lip with or without cleft palate
Overexpressing PRDM16 inhibited the epithelial-to-mesenchymal transition (EMT) of cancer cells both in vivo and in vitro by repressing the transcription of Mucin-4 (MUC4), one of the regulators of EMT in lung adenocarcinomas
Study showed that PRDM16 is over-expressed in atypical teratoid/rhabdoid tumors and has a functional role in human rhabdoid tumor cells.
In this Swedish cluster headache cohort we did not find an association with the rs2651899 variant in the PRDM16 (PR/SET domain 16) gene
Study revealed that LINC00982 and PRDM16 may serve as biomarkers or potential drug targets for the diagnosis and therapy of lung adenocarcinoma.
Multiple regression analysis showed that age, male gender, body max index, presence of obesity, type-2-diabetes mellitus, hypertension and coronary artery disease and left ventricular ejection fraction were associated with the expression levels of UCP1, PGC1alpha and PRDM16 mRNA
Our study suggests that the MEF2D, PRDM16 and ASTN2 genes from GWAS are associated with migraine susceptibility, especially migraine without aura , among Chinese patients. It appears that there is no association with serotonin receptor related genes.
High PRDM16 expression is a significant predictive marker for poor prognosis in adult AML patients.
Prdm16 interacts with the transcription factor Hlx, which is stabilized in response to beta3-adrenergic signaling, to increase thermogenic gene expression and mitochondrial biogenesis in subcutaneous WAT.
Flow cytometric analysis and western blot analysis of apoptosisassociated proteins indicated that PRDM16 has an antiapoptotic role in prostatic cancer cells. In addition, the spliced form, sPRDM16/MEL1S, was detected to be overexpressed in PCa cell lines. In conclusion, the present study indicated an important oncogenic role in prostate cancer.
A single risk variant, rs2651899 in PRDM16, was significantly associated with efficacy of triptans in migraine patients
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.
Results show that PRDM16 overexpression was highly recurrent in de novo paediatric AML and is associated with adverse outcome
PRDM16 might contribute to maintain adipose tissue "white fat" gene expression profile and systemic metabolic homeostasis.
EVI1 and MEL1 are homolog genes whose transcriptional activations by chromosomal translocations have roles in Japanese pediatric acute myeloid leukemia
Three novel loci were identified in East Asians with cardiac arrhythmias: rs2483280 (PRDM16 locus) and rs335206 (PRDM6 locus) were associated with QRS duration; and rs17026156 (SLC8A1 locus) correlated with PR interval.
Genetic analyses uncovered the importance of the PRDM16 gene in the regulation of lean body mass.
MED1 is required for optimal PRDM16-induced Ucp1 expression
GTF2IRD1 represses the transcription of transforming growth factor beta-dependent pro-fibrosis genes by recruiting PRDM16 and EHMT1 onto their promoter/enhancer regions.
the density of sympathetic projections is dependent on PRDM16 in adipocytes, providing another potential mechanism underlying the metabolic benefits mediated by PRDM16.
It is a key factor that induces the differentiation of skeletal muscle precursors to brown adipocytes and simultaneously inhibits myogenic differentiation.
Study in mice shows that after 24 h of food deprivation, subcutaneous inguinal white fat takes on many of the morphological and molecular characteristics of visceral fat to preserve energy via miR-149-3p-mediated suppression of PRDM16.
PexRAP also interacts with PPARgamma, as well as PRDM16, a critical transcriptional regulator of thermogenesis, and disrupts the PRDM16-PPARgamma complex, providing a potential mechanism for PexRAP-mediated inhibition of adipocyte browning.
Consecutive breeding to Flpe and Emx1(IREScre) deleter mice spatially restricted Prdm16 loss to regions of the forebrain expressing the homeobox gene Emx1.
Prdm16 is required for adult neural stem cell maintenance and neurogenesis as well as the formation of ependymal cells
A single subtype of ganglion cell appears to be uniquely marked by Prdm16 expression. While the precise identity of these ganglion cells is unclear, they most resemble the G9 subtype described by Volgyi and colleagues in 2009.
Gelidium elegans stimulates the expression of PRDM16 and UCP-1 Protein in brown adipose tissue and suppresses hyperglycemia in high-fat diet mice.
Both gain- and loss-of-function studies showed that an accumulation of the CCAAT/enhancer binding protein-beta (C/EBP-beta) protein, which cooperates with dominant transcriptional co-regulator PR domain containing 16 (PRDM16) to determine brown/beige adipocyte lineage, is essential for the enhanced adipocyte browning caused by the loss of ZIP13
Prdm16 plays an important role in dynamic cellular redox changes in developing neocortex during neural differentiation.
Together, these data indicate that PRDM16 diminishes responsiveness to type I interferon in adipose cells to promote thermogenic and mitochondrial function.
the cellular levels of alpha-ketoglutarate (alphaKG), a key metabolite required for TET-mediated DNA demethylation, were profoundly increased and required for active DNA demethylation of the Prdm16 promoter.
We further show that Cdkn1c is required for post-transcriptional accumulation of the brown fat determinant PR domain containing 16 (PRDM16) and that CDKN1C and PRDM16 co-localise to the nucleus of rare label-retaining cell within iBAT.
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 and PPARgamma promoters
PRDM16 deficiency in BAT reduces MED1 binding at PRDM16 target sites and causes a fundamental change in chromatin architecture at key brown fat-selective genes
Prdm16 and Prdm3 control postnatal BAT identity and function.
Study reveals that Prdm16 expression is regulated through Gcn5/PCAF during brown adipogenesis.
these studies define the transcriptional pathways involved in HOXB4 HSC expansion in vivo and identify repression of Prdm16 transcription as a mechanism by which expanding HSCs avoid leukemic transformation.
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