ACSL4 anticorps (AA 236-267)

N° du produit ABIN389113

Détail du produit anti-ACSL4 anticorps

Antigène: ACSL4 (Acyl-CoA Synthetase Long-Chain Family Member 4 (ACSL4))

Épitope: AA 236-267

Reactivité: Humain

Hôte: Lapin

Clonalité: Polyclonal

Conjugué: Cet anticorp ACSL4 est non-conjugé

Application: Western Blotting (WB), Immunohistochemistry (Paraffin-embedded Sections) (IHC (p))

Purification: This antibody is prepared by Saturated Ammonium Sulfate (SAS) precipitation followed by dialysis against PBS.

Immunogène: This ACSL4 (FACL4) antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 236-267 amino acids from the Central region of human ACSL4 (FACL4).

Clone: RB04697

Isotype: Ig Fraction

Information d'application

Indications d'application: WB: 1:1000. IHC-P: 1:25

Restrictions: For Research Use only

Stockage

Format: Liquid

Buffer: Purified polyclonal antibody supplied in PBS with 0.09 % (W/V) sodium azide.

Agent conservateur: Sodium azide

Précaution d'utilisation: This product contains Sodium azide: a POISONOUS AND HAZARDOUS SUBSTANCE which should be handled by trained staff only.

Stock: 4 °C,-20 °C

Stockage commentaire: Maintain refrigerated at 2-8 °C for up to 6 months. For long term storage store at -20 °C in small aliquots to prevent freeze-thaw cycles.

Date de péremption: 6 months

Références pour anticorps anti-ACSL4 (ABIN389113)

Shinjo, Jiang, Nameta, Suzuki, Kanai, Nomura, Goda: "Disruption of the mitochondria-associated ER membrane (MAM) plays a central role in palmitic acid-induced insulin resistance." dans: Experimental cell research, Vol. 359, Issue 1, pp. 86-93, (2017) (PubMed).

Pera, Larrea, Guardia-Laguarta, Montesinos, Velasco, Agrawal, Xu, Chan, Di Paolo, Mehler, Perumal, Macaluso, Freyberg, Acin-Perez, Enriquez, Schon, Area-Gomez: "Increased localization of APP-C99 in mitochondria-associated ER membranes causes mitochondrial dysfunction in Alzheimer disease." dans: The EMBO journal, Vol. 36, Issue 22, pp. 3356-3371, (2017) (PubMed).

Marzesco, Flötenmeyer, Bühler, Obermüller, Staufenbiel, Jucker, Baumann: "Highly potent intracellular membrane-associated Aβ seeds." dans: Scientific reports, Vol. 6, pp. 28125, (2016) (PubMed).

Williamson, Wong, Bozidis, Zhang, Colberg-Poley et al.: "Isolation of Endoplasmic Reticulum, Mitochondria, and Mitochondria-Associated Membrane and Detergent Resistant Membrane Fractions from Transfected Cells and from Human Cytomegalovirus-Infected ..." dans: Current protocols in cell biology, Vol. 68, pp. 3.27.1-33, (2016) (PubMed).

Zhang, Hildreth, Colberg-Poley: "Human cytomegalovirus inhibits apoptosis by proteasome-mediated degradation of Bax at endoplasmic reticulum-mitochondrion contacts." dans: Journal of virology, Vol. 87, Issue 10, pp. 5657-68, (2013) (PubMed).

Zhang, Williamson, Wong, Bullough, Brown, Hathout, Colberg-Poley: "Quantitative proteomic analyses of human cytomegalovirus-induced restructuring of endoplasmic reticulum-mitochondrial contacts at late times of infection." dans: Molecular & cellular proteomics : MCP, Vol. 10, Issue 10, pp. M111.009936, (2011) (PubMed).

Horner, Liu, Park, Briley, Gale: "Mitochondrial-associated endoplasmic reticulum membranes (MAM) form innate immune synapses and are targeted by hepatitis C virus." dans: Proceedings of the National Academy of Sciences of the United States of America, Vol. 108, Issue 35, pp. 14590-5, (2011) (PubMed).

Williamson, Zhang, Colberg-Poley: "The human cytomegalovirus protein UL37 exon 1 associates with internal lipid rafts." dans: Journal of virology, Vol. 85, Issue 5, pp. 2100-11, (2011) (PubMed).

Rodriguez, Bhat, Meloni, Ladd, Leslie, Doyne, Renieri, Dupont, Stevenson, Schwartz, Srivastava: "Intellectual disability, midface hypoplasia, facial hypotonia, and Alport syndrome are associated with a deletion in Xq22.3." dans: American journal of medical genetics. Part A, Vol. 152A, Issue 3, pp. 713-7, (2010) (PubMed).

Area-Gomez, de Groof, Boldogh, Bird, Gibson, Koehler, Yu, Duff, Yaffe, Pon, Schon: "Presenilins are enriched in endoplasmic reticulum membranes associated with mitochondria." dans: The American journal of pathology, Vol. 175, Issue 5, pp. 1810-6, (2009) (PubMed).

Simmen, Aslan, Blagoveshchenskaya, Thomas, Wan, Xiang, Feliciangeli, Hung, Crump, Thomas: "PACS-2 controls endoplasmic reticulum-mitochondria communication and Bid-mediated apoptosis." dans: The EMBO journal, Vol. 24, Issue 4, pp. 717-29, (2005) (PubMed).

Détails sur ACSL4

Antigène: ACSL4 (Acyl-CoA Synthetase Long-Chain Family Member 4 (ACSL4))

Autre désignation: ACSL4 (FACL4) (ACSL4 Produits)

Synonymes: anticorps acsl4, anticorps zgc:66186, anticorps ACSL4, anticorps ACS4, anticorps FACL4, anticorps LACS4, anticorps MRX63, anticorps MRX68, anticorps 9430020A05Rik, anticorps AU018108, anticorps Facl4, anticorps Lacs4, anticorps Acs4, anticorps acs4, anticorps acsl3, anticorps facl4, anticorps lacs4, anticorps mrx63, anticorps mrx68, anticorps T32A16.20, anticorps T32A16_20, anticorps long-chain acyl-CoA synthetase 4, anticorps acyl-CoA synthetase long chain family member 4a, anticorps acyl-CoA synthetase long-chain family member 4, anticorps acyl-CoA synthetase long chain family member 4, anticorps AcsL4, anticorps acyl-CoA synthetase long chain family member 3, anticorps Long-chain-fatty-acid--CoA ligase 4, anticorps acyl-CoA synthetase long-chain family member 4 S homeolog, anticorps AMP-dependent synthetase and ligase family protein, anticorps acsl4a, anticorps ACSL4, anticorps acsL4, anticorps acsl3, anticorps acsl4, anticorps Acsl4, anticorps acsl4.S, anticorps LACS4

Sujet: Long chain acyl-CoA synthetase (LACS), or long chain fatty acid-CoA ligase (FACL), converts free long chain fatty acids into fatty acyl-CoA esters, key intermediates in the synthesis of complex lipids. The FACL4 gene encodes a form of LACS and is expressed in several tissues, including brain. FACL4 cDNA from brain encodes a gene product that shows preference for arachidonic acid as a substrate when expressed in mammalian cells.1 The sequence of the predicted 670-amino acid human protein is 97 % identical to that of rat ACS4. FACL4 is highly expressed in adult human brain, especially in the cerebellum and hippocampus, similar to the mouse.2 A strong cytoplasmic staining was found in the Purkinje and granular cells of the cerebellum and the pyramidal layer of hippocampus, indicating that FACL4 is specifically expressed in neurons and not in glial cells. Two patients with Alport syndrome, elliptocytosis, and mental retardation carried a large deletion of the COL4A5 region that included FACL4.3 The absence of FACL4 might play a role in the development of mental retardation or other signs associated with Alport syndrome. Two point mutations, 1 missense and 1 splice site change, were reported in the FACL4 gene in 2 families with nonspecific mental retardation.2 Analysis of enzymatic activity in lymphoblastoid cell lines of affected individuals revealed low levels compared with normal cells, indicating that both mutations are null mutations.

Poids moléculaire: 79188

ID gène: 2182

NCBI Accession: NP_004449, NP_075266

UniProt: O60488