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Merck
모든 사진(1)

주요 문서

SAB2100035

Sigma-Aldrich

Anti-ACSL4 antibody produced in rabbit

affinity isolated antibody

동의어(들):

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 코드:
12352203
NACRES:
NA.41

생물학적 소스

rabbit

Quality Level

결합

unconjugated

항체 형태

affinity isolated antibody

항체 생산 유형

primary antibodies

클론

polyclonal

형태

buffered aqueous solution

분자량

74 kDa

종 반응성

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

농도

0.5 mg - 1 mg/mL

기술

western blot: suitable

UniProt 수납 번호

배송 상태

wet ice

저장 온도

−20°C

타겟 번역 후 변형

unmodified

유전자 정보

human ... ACSL4(2182)

일반 설명

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.

면역원

Synthetic peptide directed towards the N terminal region of human ACSL4

애플리케이션

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

생화학적/생리학적 작용

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.

서열

Synthetic peptide located within the following region: AKRIKAKPTSDKPGSPYRSVTHFDSLAVIDIPGADTLDKLFDHAVSKFGK

물리적 형태

Purified antibody supplied in 1x PBS buffer with 0.09% (w/v) sodium azide and 2% sucrose.

면책조항

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


시험 성적서(COA)

제품의 로트/배치 번호를 입력하여 시험 성적서(COA)을 검색하십시오. 로트 및 배치 번호는 제품 라벨에 있는 ‘로트’ 또는 ‘배치’라는 용어 뒤에서 찾을 수 있습니다.

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문서 라이브러리 방문

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)
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
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)

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