Mouse CIDEA blocking peptide (CDBP0803)

Synthetic Mouse CIDEA blocking peptide for BL, WB

Product Overview
mCIDE - A ( C - term ) peptide ( mouse )
Target
CIDE A
Nature
Synthetic
Species Reactivity
Mouse
Tag/Conjugate
Unconjugated
Procedure
None
Concentration
0.2 mg/ml
Size
50 μg
Buffer
PBS with 0.1% BSA 0.02% sodium azide pH7.2
Preservative
0.02% Sodium Azide
Storage
Upon Receipt - Keep as concentrated solution. Aliquot and store at -20℃ or below. Avoid freeze-thaw cycles.
UniProt ID
Antigen Description
This gene encodes the homolog of the mouse protein Cidea that has been shown to activate apoptosis. This activation of apoptosis is inhibited by the DNA fragmentation factor DFF45 but not by caspase inhibitors. Mice that lack functional Cidea have higher metabolic rates, higher lipolysis in brown adipose tissue and higher core body temperatures when subjected to cold. These mice are also resistant to diet-induced obesity and diabetes. This suggests that in mice this gene product plays a role in thermogenesis and lipolysis. Alternatively spliced transcripts have been identified. [provided by RefSeq, Aug 2010]
Function
protein homodimerization activity;
Synonyms
CIDEA; cell death-inducing DFFA-like effector a; CIDE-A; cell death activator CIDE-A;

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References


Comparative actions of omega-3 fatty acids on in-vitro lipid droplet formation

PROSTAGLANDINS LEUKOTRIENES AND ESSENTIAL FATTY ACIDS

Authors: Barber, Elizabeth; Sinclair, Andrew J.; Cameron-Smith, David

Storage of fat into lipid droplets (LDs) is the key step in adipogenesis. Previously the omega-3 polyunsaturated fatty acid (n-3PUFA) eicosapentaenoic acid (EPA; C20:5n-3) has been shown to suppress LD formation, yet the actions of other n-3PUFA is unknown. Here, we examined the impact of the three major long chain n-3PUFA; EPA, docosapentaenoic acid (DPA; C22:5n-3) and docosahexaenoic acid (DHA; C22:6n-3) on LD formation in 3T3-L1 adipocytes. Cells were supplemented with 100 mu M fatty acid during differentiation. All n-3PUFA significantly reduced LD formation and the metabolic disorder marker, SCD1, in comparison to stearic acid (STA; C18:0). This action was more potent for DHA than either EPA or DPA. Furthermore, DHA significantly increased lipolysis and ATGL gene and protein expression but reduced the gene expression of three proteins related to LD formation (Perilipin A, Caveolin-1 and Cidea), compared with other n-3PUFA. Thus, DHA, above EPA and DPA, markedly suppressed fat storage in LDs in in-vitro adipocytes. Crown Copyright (C) 2013 Published by Elsevier Ltd. All rights reserved.

Improved glucose metabolism by Eragrostis tef potentially through beige adipocyte formation and attenuating adipose tissue inflammation

PLOS ONE

Authors: Lemecha, Mengistu; Morino, Katsutaro; Seifu, Daniel; Imamura, Takeshi; Nakagawa, Fumiyuki; Nagata, Aki; Okamato, Takuya; Sekine, Osamu; Ugi, Satoshi; Maegawa, Hiroshi

Background Teff is a staple food in Ethiopia that is rich in dietary fiber. Although gaining popularity in Western countries because it is gluten-free, the effects of teff on glucose metabolism remain unknown. Aim To evaluate the effects of teff on body weight and glucose metabolism compared with an isocaloric diet containing wheat. Results Mice fed teff weighed approximately 13% less than mice fed wheat (p < 0.05). The teff-based diet improved glucose tolerance compared with the wheat group with normal chow but not with a high-fat diet. Reduced adipose inflammation characterized by lower expression of TNF alpha, Mcp1, and CD11c, together with higher levels of cecal short chain fatty acids such as acetate, compared with the control diet containing wheat after 14 weeks of dietary treatment. In addition, beige adipocyte formation, characterized by increased expression of Ucp-1 (similar to 7-fold) and Cidea (similar to 3-fold), was observed in the teff groups compared with the wheat group. Moreover, a body-weight matched experiment revealed that teff improved glucose tolerance in a manner independent of body weight reduction after 6 weeks of dietary treatment. Enhanced beige adipocyte formation without improved adipose inflammation in a body-weight matched experiment suggests that the improved glucose metabolism was a consequence of beige adipocyte formation, but not solely through adipose inflammation. However, these differences between teff- and wheat-containing diets were not observed in the high-fat diet group. Conclusions Teff improved glucose tolerance likely by promoting beige adipocyte formation and improved adipose inflammation.

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