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Merck
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Key Documents

SAB2701949

Sigma-Aldrich

Anti-ACSL4 (C-terminal) antibody produced in rabbit

Sinónimos:

FACL4, LACS4, MRX63, MRX68

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About This Item

UNSPSC Code:
12352203
NACRES:
NA.41

biological source

rabbit

Quality Level

100

conjugate

unconjugated

antibody form

purified immunoglobulin

antibody product type

primary antibodies

clone

polyclonal

form

liquid

mol wt

74 kDa

species reactivity

mouse, rat, human

concentration

1 mg/mL

technique(s)

immunocytochemistry: suitable
immunofluorescence: suitable
immunohistochemistry (formalin-fixed, paraffin-embedded sections): suitable
immunoprecipitation (IP): suitable
western blot: 500-10000

UniProt accession no.

O60488

shipped in

wet ice

storage temp.

−20°C

Gene Information

human ... ACSL4(2182)

Immunogen

Synthetic peptide corresponding to a region within amino acids 649 and 711 of FACL4 (Uniprot ID#O60488)

Application

Suggested starting dilutions are as follows: ICC/IF: 1:100-1:1000, IHC-P: 1:100-1:1000, IP: 1:1000-1:5000, WB: 1:500-1:10000. Not yet tested in other applications. Optimal working dilutions should be determined experimentally by the end user.

Biochem/physiol Actions

The protein encoded by this gene 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 2 transcript variants. [provided by RefSeq]

Features and Benefits

Evaluate our antibodies with complete peace of mind. If the antibody does not perform in your application, we will issue a full credit or replacement antibody. Learn more.

Physical form

1XPBS, 20% Glycerol (pH7). 0.01% Thimerosal was added as a preservative.

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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pictograms

Exclamation mark
GHS07

signalword

Warning

hcodes

H317,H412

Hazard Classifications

Aquatic Chronic 3 - Skin Sens. 1

Storage Class

12 - Non Combustible Liquids

wgk_germany

WGK 2

flash_point_f

Not applicable

flash_point_c

Not applicable

Certificados de análisis (COA)

Busque Certificados de análisis (COA) introduciendo el número de lote del producto. Los números de lote se encuentran en la etiqueta del producto después de las palabras «Lot» o «Batch»

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Dadi Jiang et al.
Nature communications, 15(1), 4114-4114 (2024-05-16)
Cellular sensitivity to ferroptosis is primarily regulated by mechanisms mediating lipid hydroperoxide detoxification. We show that inositol-requiring enzyme 1 (IRE1α), an endoplasmic reticulum (ER) resident protein critical for the unfolded protein response (UPR), also determines cellular sensitivity to ferroptosis. Cancer
Zhipeng Li et al.
Nature chemical biology, 18(7), 751-761 (2022-06-01)
The selenoprotein glutathione peroxidase 4 (GPX4) prevents ferroptosis by converting lipid peroxides into nontoxic lipid alcohols. GPX4 has emerged as a promising therapeutic target for cancer treatment, but some cancer cells are resistant to ferroptosis triggered by GPX4 inhibition. Using
Leslie Magtanong et al.
Cell chemical biology, 26(3), 420-432 (2019-01-29)
The initiation and execution of cell death can be regulated by various lipids. How the levels of environmental (exogenous) lipids impact cell death sensitivity is not well understood. We find that exogenous monounsaturated fatty acids (MUFAs) potently inhibit the non-apoptotic
Jorge Montesinos et al.
The EMBO journal, 39(20), e103791-e103791 (2020-09-01)
The link between cholesterol homeostasis and cleavage of the amyloid precursor protein (APP), and how this relationship relates to Alzheimer's disease (AD) pathogenesis, is still unknown. Cellular cholesterol levels are regulated through crosstalk between the plasma membrane (PM), where most

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