Adipogenesis Marker Antibody Sampler Kit #12589
Product Information
Kit Usage Information
Protocols
- 2120: Western Blotting
- 2435: Western Blotting, Immunohistochemistry (Paraffin), Immunofluorescence, ChIP Magnetic, Chromatin IP-seq
- 2789: Western Blotting
- 3180: Western Blotting, Immunoprecipitation (Agarose), Immunohistochemistry (Paraffin), Immunofluorescence, Flow
- 3676: Western Blotting, Immunoprecipitation (Agarose), Immunohistochemistry (Paraffin), Immunofluorescence, Flow
- 7074: Western Blotting
- 8178: Western Blotting, Immunoprecipitation (Magnetic), Immunohistochemistry (Paraffin), Immunofluorescence, Flow
- 9349: Western Blotting, Immunoprecipitation (Agarose), Immunohistochemistry (Paraffin), Immunofluorescence, Immunofluorescence
Product Description
The Adipogenesis Marker Antibody Sampler Kit provides an economical means to evaluate proteins involved in the regulation of adipogenesis. The kit includes enough antibody to perform two western blot experiments with each primary antibody.
Background
Adipocytes are the primary cellular component of adipose tissue and play a key role in the storage of triacylglycerol. Adipogenesis is the cellular process where preadipocytes differentiate into adipocytes.
Fatty acid binding proteins (FABPs) act as cytoplasmic lipid chaperones by binding fatty acids and lipids for transport to various cellular pathways (1,2). The predominant fatty acid binding protein found in adipocytes is FABP4.
Adiponectin is an adipokine expressed exclusively in brown and white adipocytes and is secreted into the blood. It exists in three major forms: a low molecular weight trimer, a medium molecular weight hexamer and a high molecular weight multimer (3). Decreased adiponectin levels are seen in obese and insulin-resistant mice and humans (4), suggesting that this adipokine is critical for maintenance of insulin sensitivity.
Peroxisome proliferator-activated receptor γ (PPARγ) is a transcriptional activator preferentially expressed in adipocytes, vascular smooth muscle cells, and macrophages (5,6).
Acetyl-CoA carboxylase (ACC) is a key fatty acid biosynthesis and oxidation enzyme that is responsible for the carboxylation of acetyl-CoA to malonyl-CoA, (7). Phosphorylation of acetyl-CoA carboxylase by AMPK at Ser79 or by PKA at Ser1200 inhibits ACC enzymatic activity (8). ACC is a potential target of anti-obesity drugs (9,10).
CCAAT/enhancer-binding proteins (C/EBPs) transcription factors are critical for cellular differentiation, terminal function, and the inflammatory response (11). Phosphorylation of C/EBPα at Thr222, Thr226, and Ser230 by GSK-3 may be required for adipogenesis (12).
Perilipin localizes to the periphery of lipid droplets and serves as a protective coating against lipases. Evidence suggests that PKA regulates lipolysis by phosphorylating perilipin (13-17), resulting in a conformational change that exposes lipid droplets to endogenous, hormone-sensitive lipases (14). Hence, perilipin plays a pivotal role in lipid storage (14,17).
Fatty acid synthase (FASN) catalyzes the synthesis of long-chain fatty acids from acetyl-CoA and malonyl-CoA. FASN is active as a homodimer with seven different catalytic activities and produces lipids in the liver for export to metabolically active tissues or storage in adipose tissue. In most other human tissues, FASN is minimally expressed since they rely on circulating fatty acids for new structural lipid synthesis (18).
Fatty acid binding proteins (FABPs) act as cytoplasmic lipid chaperones by binding fatty acids and lipids for transport to various cellular pathways (1,2). The predominant fatty acid binding protein found in adipocytes is FABP4.
Adiponectin is an adipokine expressed exclusively in brown and white adipocytes and is secreted into the blood. It exists in three major forms: a low molecular weight trimer, a medium molecular weight hexamer and a high molecular weight multimer (3). Decreased adiponectin levels are seen in obese and insulin-resistant mice and humans (4), suggesting that this adipokine is critical for maintenance of insulin sensitivity.
Peroxisome proliferator-activated receptor γ (PPARγ) is a transcriptional activator preferentially expressed in adipocytes, vascular smooth muscle cells, and macrophages (5,6).
Acetyl-CoA carboxylase (ACC) is a key fatty acid biosynthesis and oxidation enzyme that is responsible for the carboxylation of acetyl-CoA to malonyl-CoA, (7). Phosphorylation of acetyl-CoA carboxylase by AMPK at Ser79 or by PKA at Ser1200 inhibits ACC enzymatic activity (8). ACC is a potential target of anti-obesity drugs (9,10).
CCAAT/enhancer-binding proteins (C/EBPs) transcription factors are critical for cellular differentiation, terminal function, and the inflammatory response (11). Phosphorylation of C/EBPα at Thr222, Thr226, and Ser230 by GSK-3 may be required for adipogenesis (12).
Perilipin localizes to the periphery of lipid droplets and serves as a protective coating against lipases. Evidence suggests that PKA regulates lipolysis by phosphorylating perilipin (13-17), resulting in a conformational change that exposes lipid droplets to endogenous, hormone-sensitive lipases (14). Hence, perilipin plays a pivotal role in lipid storage (14,17).
Fatty acid synthase (FASN) catalyzes the synthesis of long-chain fatty acids from acetyl-CoA and malonyl-CoA. FASN is active as a homodimer with seven different catalytic activities and produces lipids in the liver for export to metabolically active tissues or storage in adipose tissue. In most other human tissues, FASN is minimally expressed since they rely on circulating fatty acids for new structural lipid synthesis (18).
- Tuncman, G. et al. (2006) Proc Natl Acad Sci U S A 103, 6970-5.
- Haunerland, N.H. and Spener, F. (2004) Prog Lipid Res 43, 328-49.
- Kadowaki, T. et al. (2006) J Clin Invest 116, 1784-92.
- Hu, E. et al. (1996) J Biol Chem 271, 10697-703.
- Tontonoz, P. et al. (1995) Curr Opin Genet Dev 5, 571-6.
- Rosen, E.D. et al. (1999) Mol Cell 4, 611-7.
- Castle, J.C. et al. (2009) PLoS One 4, e4369.
- Ha, J. et al. (1994) J Biol Chem 269, 22162-8.
- Abu-Elheiga, L. et al. (2001) Science 291, 2613-6.
- Levert, K.L. et al. (2002) J Biol Chem 277, 16347-50.
- Lekstrom-Himes, J. and Xanthopoulos, K.G. (1998) J Biol Chem 273, 28545-8.
- Ross, S.E. et al. (1999) Mol Cell Biol 19, 8433-41.
- Greenberg, A.S. et al. (1991) J Biol Chem 266, 11341-6.
- Brasaemle, D.L. (2007) J Lipid Res 48, 2547-59.
- Ducharme, N.A. and Bickel, P.E. (2008) Endocrinology 149, 942-9.
- Egan, J.J. et al. (1990) J Biol Chem 265, 18769-75.
- Brasaemle, D.L. et al. (2009) Mol Cell Biochem 326, 15-21.
- Katsurada, A. et al. (1990) Eur J Biochem 190, 427-33.
限制使用
除非 CST 的合法授书代表以书面形式书行明确同意，否书以下条款适用于 CST、其关书方或分书商提供的书品。 任何书充本条款或与本条款不同的客书条款和条件，除非书 CST 的合法授书代表以书面形式书独接受， 否书均被拒书，并且无效。
专品专有“专供研究使用”的专专或专似的专专声明， 且未专得美国食品和专品管理局或其他外国或国内专管机专专专任何用途的批准、准专或专可。客专不得将任何专品用于任何专断或治专目的， 或以任何不符合专专声明的方式使用专品。CST 专售或专可的专品提供专作专最专用专的客专，且专用于研专用途。将专品用于专断、专防或治专目的， 或专专售（专独或作专专成）或其他商专目的而专专专品，均需要 CST 的专独专可。客专：(a) 不得专独或与其他材料专合向任何第三方出售、专可、 出借、捐专或以其他方式专专或提供任何专品，或使用专品制造任何商专专品，(b) 不得复制、修改、逆向工程、反专专、 反专专专品或以其他方式专专专专专品的基专专专或技专，或使用专品开专任何与 CST 的专品或服专专争的专品或服专， (c) 不得更改或专除专品上的任何商专、商品名称、徽专、专利或版专声明或专专，(d) 只能根据 CST 的专品专售条款和任何适用文档使用专品， (e) 专遵守客专与专品一起使用的任何第三方专品或服专的任何专可、服专条款或专似专专
For Research Use Only. Not for Use in Diagnostic Procedures.
Cell Signaling Technology is a trademark of Cell Signaling Technology, Inc.
U.S. Patent No. 7,429,487, foreign equivalents, and child patents deriving therefrom.
All other trademarks are the property of their respective owners. Visit our
Trademark Information page.