Anti-ACSL5 Antibody, Rabbit Polyclonal sinobiological 203014-T08

$143.00
In stock
SKU
203014-T08
Catalog No.SizePrice (USD)
203014-T08-5050 µL$147.96
203014-T08-100100 µL$251.64
203014-T08-200200 µL$355.32

General Information

Product nameAnti-ACSL5 Antibody, Rabbit Polyclonal
Validated applicationsIHC-P (FAQ Protocol)
Species reactivityReacts with: Human
SpecificityHuman ACSL5
ImmunogenE. coli-derived Human ACSL5 fragment
PreparationProduced in rabbits immunized with E. coli-derived Human ACSL5 fragment, and purified by antigen affinity chromatography.
SourcePolyclonal Rabbit IgG
PurificationProtein A & Antigen Affinity
FormulationPBS, pH7.0 with 0.03% Proclin300
ConjugateUnconjugated
FormLiquid
ShippingThis antibody is shipped as liquid solution at ambient temperature. Upon receipt, store it immediately at the temperature recommended below.
StorageThis antibody can be stored at 2℃-8℃ for one month without detectable loss of activity. Antibody products are stable for twelve months from date of receipt when stored at -20℃ to -80℃. Avoid repeated freeze-thaw cycles.

Synonyms: Anti-ACS2 Antibody; Anti-ACS5 Antibody; Anti-DIAR13 Antibody; Anti-FACL5 Antibody; Anti-UNQ633/PRO1250 Antibody

Image / Experimental Information

Image 1 DescriptionImmunochemical staining of human ACSL5 in human liver with rabbit polyclonal antibody at 1:100 dilution, formalin-fixed paraffin embedded sections.
Image 1 Alt TextHuman ACSL5 Immunohistochemistry(IHC) 22013
Image 1 URLSource image

Background Information

Full Nameacyl-CoA synthetase long-chain family member 5
DescriptionLong-chain acyl-CoA synthetases (ACSLs) activate fatty acids (FAs: C12-C20), by thioesterification with Coenzyme A (CoA), generating FA-CoAs. Acyl-CoA synthetase 5 (ACSL5), a mitochondrially localized enzyme, catalyzes the synthesis of long-chain fatty acid thioesters and is physiologically involved in pro-apoptotic sensing of enterocytes. ACSL5 is implicated in several types of cancers and has a potential prognostic value. Unlike other ACSLs, ACSL5 is downregulated in colorectal carcinomas, breast, bladder, and pancreas. However, ACSL5 is overexpressed in glioma and considered a potential therapeutic target. Besides, the fibroblast growth factor receptor 2 (FGFR2) ACSL5 chimera RNA rendered clinical gastric cancer cells resistant to treatment with FGFR inhibitors.
References
  1. Klaus C, et al. (2014) Tp53 status regulates acsl5-induced expression of mitochondrial mortalin in enterocytes and colorectal adenocarcinomas. Cell Tissue Res 357 (1): 267-278.

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