SAB1300006
Anti-PRDM16 (N-term) antibody produced in rabbit
IgG fraction of antiserum, buffered aqueous solution
Synonym(s):
Anti-PFM13, MEL1
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About This Item
UNSPSC Code:
12352203
NACRES:
NA.41
Recommended Products
biological source
rabbit
Quality Level
conjugate
unconjugated
antibody form
IgG fraction of antiserum
antibody product type
primary antibodies
clone
polyclonal
form
buffered aqueous solution
species reactivity
human
technique(s)
immunohistochemistry: 1:50-1:100
indirect ELISA: 1:1000
NCBI accession no.
UniProt accession no.
shipped in
dry ice
storage temp.
−20°C
target post-translational modification
unmodified
Gene Information
human ... PRDM16(63976)
General description
PR/SET domain 16 (PRDM16) is encoded by the gene mapped to human chromosome 1p36.32. PRDM16 is a 140kDa zinc-finger protein characterized with a PR (PRD1-BF1-RIZ1 homologous)-domain. It is highly expressed in brown fat cells compared to white fat cells.
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. Purified recombinant GST fusion protein encoding N-terminal aa 13-316 of human PRDM16.
Immunogen
PRDM16 (NP_071397, 1-350)
Purified recombinant GST fusion protein encoding N-terminal aa 13-316 of human PRDM16.
Purified recombinant GST fusion protein encoding N-terminal aa 13-316 of human PRDM16.
Application
Anti-PRDM16 (N-term) antibody produced in rabbit has been used in western blotting..
Biochem/physiol Actions
PR/SET domain 16 (PRDM16) is a potential transcriptional regulator. It regulates a bidirectional cell fate switch between skeletal myoblasts and brown fat cells. The encoded protein plays an essential role in promoting adipogenesis by co-activating transcriptional function of PPARγ. PRDM16 is required for cardiac development. Thus, loss of PRDM16 gene expression leads to the development of cardiomyopathy of 1p36 deletion syndrome. Variation in the gene expression is associated with the development of migraine.
Physical form
Purified polyclonal antibody supplied in PBS with 0.09% (W/V) sodium azide.
Disclaimer
Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.
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Storage Class Code
10 - Combustible liquids
WGK
nwg
Flash Point(F)
Not applicable
Flash Point(C)
Not applicable
Certificates of Analysis (COA)
Search for Certificates of Analysis (COA) by entering the products Lot/Batch Number. Lot and Batch Numbers can be found on a product’s label following the words ‘Lot’ or ‘Batch’.
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Transcriptional Control of Brown Fat Determination by PRDM16
Seale P, et al.
Cell Metabolism, 6(1), 38-54 (2007)
Cdkn1c boosts the development of brown adipose tissue in a murine model of Silver Russell syndrome.
Van De Pette M, et al.
PLoS Genetics, 12(3), e1005916-e1005916 (2016)
Loss of PRDM16 Is Unlikely to Cause Cardiomyopathy in 1p36 Deletion Syndrome
de Leeuw N, et al.
American Journal of Human Genetics, 94(1), 153-154 (2014)
PRDM16 Controls a Brown Fat/Skeletal Muscle Switch
Seale P, et al.
Nature, 454(7207), 961-961 (2008)
Matthew Van De Pette et al.
PLoS genetics, 12(3), e1005916-e1005916 (2016-03-11)
The accurate diagnosis and clinical management of the growth restriction disorder Silver Russell Syndrome (SRS) has confounded researchers and clinicians for many years due to the myriad of genetic and epigenetic alterations reported in these patients and the lack of
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