product summary
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company name :
MyBioSource
product type :
ELISA/assay
product name :
Mouse Cell death activator CIDE-3, CIDEC ELISA Kit
catalog :
MBS9337491
quantity :
48-Strip-Wells
price :
435 USD
more info or order :
product information
catalog number :
MBS9337491
products type :
ELISA Kit
products full name :
Mouse Cell death activator CIDE-3, CIDEC ELISA Kit
products short name :
cell death-inducing DFFA-like effector c
products name syn :
Mouse Cell death activator CIDE-3 (CIDEC) ELISA kit; CIDE-3; FLJ20871; Fsp27; cell death activator CIDE-3; fat specific protein 27; cell death-inducing DFFA-like effector c
other names :
cell death activator CIDE-3; Cell death activator CIDE-3; cell death activator CIDE-3; CIDE-3alpha; fat specific gene 27; fat-specific protein FSP27; cell death-inducing DFFA-like effector protein C; cell death-inducing DFFA-like effector c; Cell death-inducing DFFA-like effector protein C; Fat-specific protein FSP27
products gene name :
CIDEC
other gene names :
Cidec; Cidec; Fsp27; CIDE-3; Fsp27
uniprot entry name :
CIDEC_MOUSE
reactivity :
Mouse
storage stability :
Store all reagents at 2-8 degree C
ncbi gi num :
30410022
ncbi acc num :
NP_848460.1
ncbi gb acc num :
NM_178373.3
uniprot acc num :
P56198
ncbi mol weight :
27,324 Da
uniprot summary :
CIDEC: May act as a CEBPB coactivator in white adipose tissue to control the expression of a subset of CEBPB downstream target genes, including SOCS1, SOCS3, TGFB1, TGFBR1, ID2 and XDH. Binds to lipid droplets and regulates their enlargement, thereby restricting lipolysis and favoring storage. At focal contact sites between lipid droplets, promotes directional net neutral lipid transfer from the smaller to larger lipid droplets. The transfer direction may be driven by the internal pressure difference between the contacting lipid droplet pair. When overexpressed in preadipocytes, induces apoptosis or increases cell susceptibility to apoptosis induced by serum deprivation or TGFB treatment. As mature adipocytes, that express high CIDEC levels, are quite resistant to apoptotic stimuli, the physiological significance of its role in apoptosis is unclear. In omental adipose tissue of obese patients matched for BMI, expression levels tend to correlate with insulin sensitivity. Expression is increased 2-3 fold in the group of patients with high insulin sensitivity, compared to the insulin- resistant group. This observation is consistent with the idea that triglyceride storage in adipocytes plays an important role in sequestering triglycerides and fatty acids away from the circulation and peripheral tissues, thus enhancing insulin sensitivity in liver and muscle. This effect is not significant in subcutaneous adipose tissue (PubMed:18509062). In subcutaneous adipose tissue of diabetic patients, tends to negatively correlate with body mass index and total fat mass, independently of insulin sensitivity (PubMed:18334488). 3 isoforms of the human protein are produced by alternative splicing. Protein type: Apoptosis. Cellular Component: endoplasmic reticulum; lipid particle; intracellular; cytosol; nucleus. Biological Process: regulation of apoptosis; regulation of transcription, DNA-dependent; transcription, DNA-dependent; apoptosis
size1 :
48-Strip-Wells
price1 :
435 USD
size2 :
96-Strip-Wells
price2 :
600
more info or order :
company information
MyBioSource
P.O. Box 153308
San Diego, CA 92195-3308
sales@mybiosource.com
https://www.mybiosource.com
1-888-627-0165
headquarters: USA
MyBioSource, LLC was orginally founded in Vancouver by three enthusiastic scientists who are passionate about providing the world with the best reagents available. Together, they form a company with a big vision known as MyBioSource. MyBioSource is now located in San Diego, California, USA.

"MyBioSource's number 1 vision is to be the world's number 1 quality reagents provider."

Our goal is to provide researchers, scientists and customers alike with a one-stop-shop for all of their reagents needs, whether it is monoclonal antibody, polyclonal antibody, recombinant protein, peptide, etc...

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