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AV41562

Sigma-Aldrich

Anti-HMGCS2 (AB1) antibody produced in rabbit

IgG fraction of antiserum, lyophilized powder

Synonym(s):

Anti-3-Hydroxy-3-methylglutaryl-coenzyme A synthase 2 (mitochondrial)

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About This Item

UNSPSC Code:
12352203

biological source

rabbit

conjugate

unconjugated

antibody form

IgG fraction of antiserum

antibody product type

primary antibodies

clone

polyclonal

form

lyophilized powder

mol wt

56 kDa

species reactivity

canine, human, horse, rat, pig, rabbit, mouse, chicken, bovine

technique(s)

western blot: suitable

immunogen sequence

FSTASAVPLAKTDTWPKDVGILALEVYFPAQYVDQTDLEKYNNVEAGKYT

NCBI accession no.

UniProt accession no.

storage temp.

−20°C

target post-translational modification

unmodified

Gene Information

human ... HMGCS2(3158)

General description

HMG-coenzyme A synthase 2 (mitochondrial) (HMGCS2) is the mitochondrial form of HMG-CoA synthase, the enzyme that catalyzes the condensation of acetyl-CoA with acetoacetyl-CoA to form HMG-CoA. HMG-CoA synthase 2 regulates and rate-limits ketone body production and mitochondrial fatty acid oxidation within liver cells and some extrahepatic tissues such as the colon.

Specificity

Anti-HMGCS2 (AB1) polyclonal antibody reacts with bovine, human, mouse, rat, canine, pig, and chicken HMG-coenzyme A synthase 2 proteins.

Immunogen

synthetic peptide corresponding to a region of human HMGCS2 with an internal ID of P24247

Application

Anti-HMGCS2 (AB1) polyclonal antibody is used to tag the HMG-coenzyme A synthase 2 for detection and quantitation by Western blotting and in plasma by immunohistochemical (IHC) techniques. It is used as a probe to determine the roles of HMG-coenzyme A synthase 2 in ketone body production and mitochondrial fatty acid oxidation within hepatic and other tissues.

Physical form

Lyophilized from PBS buffer with 2% sucrose

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

11 - Combustible Solids

wgk_germany

WGK 1

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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Chia-Wei Cheng et al.
Cell, 178(5), 1115-1131 (2019-08-24)
Little is known about how metabolites couple tissue-specific stem cell function with physiology. Here we show that, in the mammalian small intestine, the expression of Hmgcs2 (3-hydroxy-3-methylglutaryl-CoA synthetase 2), the gene encoding the rate-limiting enzyme in the production of ketone
Maria M Mihaylova et al.
Cell stem cell, 22(5), 769-778 (2018-05-05)
Diet has a profound effect on tissue regeneration in diverse organisms, and low caloric states such as intermittent fasting have beneficial effects on organismal health and age-associated loss of tissue function. The role of adult stem and progenitor cells in
Ubaldo E Martinez-Outschoorn et al.
Cell cycle (Georgetown, Tex.), 11(21), 3964-3971 (2012-10-23)
We have previously proposed that catabolic fibroblasts generate mitochondrial fuels (such as ketone bodies) to promote the anabolic growth of human cancer cells and their metastasic dissemination. We have termed this new paradigm "two-compartment tumor metabolism." Here, we further tested
Semir Beyaz et al.
Nature, 531(7592), 53-58 (2016-03-05)
Little is known about how pro-obesity diets regulate tissue stem and progenitor cell function. Here we show that high-fat diet (HFD)-induced obesity augments the numbers and function of Lgr5(+) intestinal stem cells of the mammalian intestine. Mechanistically, a HFD induces
Victoire Gouirand et al.
The EMBO journal, 41(9), e110466-e110466 (2022-03-22)
Pancreatic ductal adenocarcinoma (PDA) tumor cells are deprived of oxygen and nutrients and therefore must adapt their metabolism to ensure proliferation. In some physiological states, cells rely on ketone bodies to satisfy their metabolic needs, especially during nutrient stress. Here

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