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SAB2100035

Sigma-Aldrich

Anti-ACSL4 antibody produced in rabbit

affinity isolated antibody

Synonym(s):

Anti-ACS4, Anti-Acyl-CoA synthetase long-chain family member 4, Anti-FACL4, Anti-LACS4, Anti-MRX63, Anti-MRX68

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About This Item

UNSPSC Code:
12352203
NACRES:
NA.41

biological source

rabbit

Quality Level

conjugate

unconjugated

antibody form

affinity isolated antibody

antibody product type

primary antibodies

clone

polyclonal

form

buffered aqueous solution

mol wt

74 kDa

species reactivity

rat, rabbit, guinea pig, mouse, bovine, human, dog, horse

concentration

0.5 mg - 1 mg/mL

technique(s)

western blot: suitable

UniProt accession no.

shipped in

wet ice

storage temp.

−20°C

target post-translational modification

unmodified

Gene Information

human ... ACSL4(2182)

General description

Acyl-CoA synthetase long-chain family member 4 (Acsl4) is encoded by the gene mapped to human chromosome Xq22.3−Xq23. Acsl4 is a member of the long-chain fatty-acid-coenzyme A ligase family. All the members of this family have different substrate specificity, subcellular localization, and tissue distribution. Alternative splicing of Acsl4 gene generates two transcript variants.

Immunogen

Synthetic peptide directed towards the N terminal region of human ACSL4

Application

Anti-ACSL4 antibody produced in rabbit has been used as a mitochondria-associated membrane (MAM) marker.

Biochem/physiol Actions

ACSL4 is an isozyme of the long-chain fatty-acid-coenzyme A ligase family. Although differing in substrate specificity, subcellular localization, and tissue distribution, all isozymes of this family convert free long-chain fatty acids into fatty acyl-CoA esters, and thereby play a key role in lipid biosynthesis and fatty acid degradation. This isozyme preferentially utilizes arachidonate as substrate. The absence of this enzyme may contribute to the mental retardation or Alport syndrome. Alternative splicing of this gene generates two transcript variants.
Long-chain fatty-acid-coenzyme A ligase family members convert free long-chain fatty acids into fatty acyl-CoA esters, and thereby facilitate lipid biosynthesis and fatty acid degradation. Acsl4 plays a critical role in ferroptosis execution. It also contributes to the dendritic spine architecture. Acsl4 isozyme preferentially utilizes arachidonate as substrate. The absence of this enzyme may contribute to the non-syndromic X-linked mental retardation or Alport syndrome.

Sequence

Synthetic peptide located within the following region: AKRIKAKPTSDKPGSPYRSVTHFDSLAVIDIPGADTLDKLFDHAVSKFGK

Physical form

Purified antibody supplied in 1x PBS buffer with 0.09% (w/v) sodium azide and 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 Code

10 - Combustible liquids

WGK

WGK 3

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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AMMECR1: a single point mutation causes developmental delay, midface hypoplasia and elliptocytosis
Andreoletti G, et al.
Journal of medical Genetics, 54(4), 269-277 (2017)
The XLMR gene ACSL4 plays a role in dendritic spine architecture
Meloni I, et al.
Neuroscience, 159, 657-669 (2009)
Acsl4 Dictates Ferroptosis Sensitivity by Shaping Cellular Lipid Composition
Doll S, et al.
Nature Chemical Biology, 13, 91-91 (2017)
N-Acetylcysteine prevents the spatial memory deficits and the redox-dependent RyR2 decrease displayed by an Alzheimer?s disease rat model
More JY, et al.
Frontiers in Aging Neuroscience, 10(4), 399-399 (2018)
Xiaojia Guo et al.
Scientific reports, 13(1), 22255-22255 (2023-12-15)
Cisplatin (CP) induces acute kidney injury (AKI) whereby proximal tubules undergo regulated necrosis. Repair is almost complete after a single dose. We now demonstrate a role for Apolipoprotein B mRNA editing enzyme, catalytic polypeptide 1 (Apobec-1) that is prominently expressed

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