ACSL5 Rabbit Pab

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Leader in Biomolecular Solutions for Life Science ACSL5 Rabbit pAb Catalog No.: A1270 1 Publications Basic Information Background Catalog No. The protein encoded by this gene is an isozyme of the long-chain fatty-acid-coenzyme A A1270 ligase family. Although differing in substrate specificity, subcellular localization, and tissue distribution, all isozymes of this family convert free long-chain fatty acids into Observed MW fatty acyl-CoA esters, and thereby play a key role in lipid biosynthesis and fatty acid 70-76kDa degradation. This isozyme is highly expressed in uterus and spleen, and in trace amounts in normal brain, but has markedly increased levels in malignant gliomas. This Calculated MW gene functions in mediating fatty acid-induced glioma cell growth. Three transcript 73kDa/75kDa/82kDa variants encoding two different isoforms have been found for this gene. Category Primary antibody Applications WB,IHC Cross-Reactivity Human, Mouse, Rat Recommended Dilutions Immunogen Information WB 1:500 - 1:2000 Gene ID Swiss Prot 51703 Q9ULC5 IHC 1:20 - 1:100 Immunogen Recombinant fusion protein containing a sequence corresponding to amino acids 500-739 of human ACSL5 (NP_057318.2). Synonyms ACSL5;ACS2;ACS5;FACL5 Contact Product Information www.abclonal.com Source Isotype Purification Rabbit IgG Affinity purification Storage Store at -20℃. Avoid freeze / thaw cycles. Buffer: PBS with 0.02% sodium azide,50% glycerol,pH7.3. Validation Data Western blot analysis of extracts of various cell lines, using ACSL5 antibody (A1270) at 1:1000 dilution. Secondary antibody: HRP Goat Anti-Rabbit IgG (H+L) (AS014) at 1:10000 dilution. Lysates/proteins: 25ug per lane. Blocking buffer: 3% nonfat dry milk in TBST. Detection: ECL Basic Kit (RM00020). Exposure time: 1s. Immunohistochemistry of paraffin- embedded rat kidney using ACSL5 antibody (A1270) at dilution of 1:100 (40x lens). Antibody | Protein | ELISA Kits | Enzyme | NGS | Service For research use only. Not for therapeutic or diagnostic purposes. Please visit http://abclonal.com for a complete listing of recommended products..

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DYSREGULATION of LONG-CHAIN ACYL-Coa SYNTHETASES in CANCER and THEIR TARGETING STRATEGIES in ANTICANCER THERAPY Md Amir Hossain1, Jun Ma2, Yong Yang1 1
Hossain et al RJLBPCS 2020 www.rjlbpcs.com Life Science Informatics Publications Original Review Article DOI: 10.26479/2020.0603.06 DYSREGULATION OF LONG-CHAIN ACYL-CoA SYNTHETASES IN CANCER AND THEIR TARGETING STRATEGIES IN ANTICANCER THERAPY Md Amir Hossain1, Jun Ma2, Yong Yang1 1. Academic Institute of Pharmaceutical Science, China Pharmaceutical University, Nanjing, China. 2. Ningxia Baoshihua Hospital, Ningxia, China. ABSTRACT: Cancer is a leading cause of death worldwide, and the number of cases globally continues to increase. Cancer is caused by certain changes in genes that are involved in controlling cell functions and cell division. Notably, metabolic dysregulation is one the hallmarks of cancer, and increases in fatty acid metabolism have been demonstrated to promote the growth and survival of a variety of cancers. In human, fatty acids either can be breakdown into acetyl-CoA through catabolic metabolism and aid in ATP generation or in the anabolic metabolism they can incorporate into triacylglycerol and phospholipid. Importantly, both of these pathways need activation of fatty acids, and the key players in this activation of fatty acids are the long-chain acyl-CoA synthetases (ACSLs) that are commonly dysregulated in cancer and associated with oncogenesis and survival. Therefore, it provides a rationale to target ACSLs in cancer. This review summarizes the current understanding of long-chain acyl-CoA synthetases in cancer and their targeting opportunities. KEYWORDS: Acyl-CoA synthetases, cancer, fatty acid, lipid metabolism. Article History: Received: April 15, 2020; Revised: May 10, 2020; Accepted: May 30, 2020. Corresponding Author: Prof. Yong Yang* Academic Institute of Pharmaceutical Science, China Pharmaceutical University, Nanjing, China.
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Flawed Phospholipid Formation Or Faulty Fatty Acid Oxidation: Determining the Cause of Mitochondrial Dysfunction in Hearts Lacking Acsl1
FLAWED PHOSPHOLIPID FORMATION OR FAULTY FATTY ACID OXIDATION: DETERMINING THE CAUSE OF MITOCHONDRIAL DYSFUNCTION IN HEARTS LACKING ACSL1 Trisha J. Grevengoed A dissertation submitted to the faculty at the University of North Carolina at Chapel Hill in partial fulfillment of the requirements for the degree of Doctor of Philosophy in the Department of Nutrition (Biochemistry) in the School of Public Health. Chapel Hill 2015 Approved by: Rosalind A. Coleman Stephen D. Hursting Liza Makowski Leslie V. Parise Steven H. Zeisel © 2015 Trisha J. Grevengoed ALL RIGHTS RESERVED ii ABSTRACT Trisha J. Grevengoed: Fatty acid activation in cardiac mitochondria: The role of ACSL1 in phospholipid formation and remodeling, substrate switching, and autophagic flux (Under the direction of Rosalind A. Coleman) Cardiovascular disease is the number one cause of death worldwide. In the heart, mitochondria provide up to 95% of energy, with most of this energy coming from metabolism of fatty acids (FA). FA must be converted to acyl-CoAs by acyl-CoA synthetases (ACS) before entry into pathways of β- oxidation or glycerolipid synthesis. ACSL1 contributes more than 90% of total cardiac ACSL activity, and mice with an inducible knockout of ACSL1 (Acsl1T-/-) have impaired cardiac FA oxidation. The effects of loss of ACSL1 on mitochondrial respiratory function, phospholipid formation, or autophagic flux have not yet been studied. Acsl1T-/- hearts contained 3-fold more mitochondria with abnormal structure and displayed lower respiratory function. Because ACSL1 exhibited a strong substrate preference for linoleate (18:2), we investigated the composition of mitochondrial phospholipids. Acsl1T-/- hearts contained 83% less tetralinoleoyl-cardiolipin (CL), the major form present in control hearts.
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Elucidating Biological Roles of Novel Murine Genes in Hearing Impairment in Africa
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ACSL5 Polyclonal Antibody Gene Symbol: ACSL5
ACSL5 polyclonal antibody Gene Symbol: ACSL5 Gene Alias: ACS2, ACS5, FACL5 Catalog Number: PAB7030 Gene Summary: The protein encoded by this gene is an Regulatory Status: For research use only (RUO) isozyme of the long-chain fatty-acid-coenzyme A ligase Product Description: Goat polyclonal antibody raised family. Although differing in substrate specificity, against synthetic peptide of ACSL5. subcellular localization, and tissue distribution, all isozymes of this family convert free long-chain fatty Immunogen: A synthetic peptide corresponding to acids into fatty acyl-CoA esters, and thereby play a key human ACSL5. role in lipid biosynthesis and fatty acid degradation. This isozyme is highly expressed in uterus and spleen, and in Sequence: C-RTQIDSLYEHIQD trace amounts in normal brain, but has markedly increased levels in malignant gliomas. This gene Host: Goat functions in mediating fatty acid-induced glioma cell growth. Three transcript variants encoding two different Theoretical MW (kDa): 82.3, 76 isoforms have been found for this gene. [provided by RefSeq] Reactivity: Human References: Applications: ELISA, WB-Ti 1. Coeliac disease is associated with impaired (See our web site product page for detailed applications expression of acyl-CoA-synthetase 5. Obermuller N, information) Keith M, Kopitz J, Autschbach F, Schirmacher P, Protocols: See our web site at Gassler N. Int J Colorectal Dis. 2006 Mar;21(2):130-4. http://www.abnova.com/support/protocols.asp or product Epub 2005 Apr 5. page for detailed protocols Specificity: This antibody is expected to recognize isoform a (NP_057318.2) and isoform b (NP_976313.1 and NP_976314.1). Form: Liquid Purification: Antigen affinity purification Concentration: 0.5 mg/mL Recommend Usage: ELISA (1:16000) Western Blot (1-3 ug/mL) The optimal working dilution should be determined by the end user.
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NIH Public Access Author Manuscript Future Lipidol
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ACSL5 (Human) IP-WB Antibody Pair
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www.aging-us.com AGING 2021, Vol. 13, No. 12 Research Paper Immune infiltration and a ferroptosis-associated gene signature for predicting the prognosis of patients with endometrial cancer Yin Weijiao1,2, Liao Fuchun1, Chen Mengjie1, Qin Xiaoqing1, Lai Hao3, Lin Yuan3, Yao Desheng1 1Department of Gynecologic Oncology, Guangxi Medical University Cancer Hospital, Nanning, Guangxi Zhuang Autonomous Region 530021, PR China 2Henan Key Laboratory of Cancer Epigenetics, Cancer Hospital, The First Affiliated Hospital, College of Clinical Medicine, Medical College of Henan University of Science and Technology, Luoyang, PR China 3Department of Gastrointestinal Surgery, Guangxi Medical University Cancer Hospital, Nanning, Guangxi Zhuang Autonomous Region 530021, PR China Correspondence to: Yao Desheng; email: [email protected] Keywords: ferroptosis, endometrial cancer, prognosis Received: March 24, 2021 Accepted: June 4, 2021 Published: June 24, 2021 Copyright: © 2021 Weijiao et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. ABSTRACT Ferroptosis, a form of programmed cell death induced by excess iron-dependent lipid peroxidation product accumulation, plays a critical role in cancer. However, there are few reports about ferroptosis in endometrial cancer (EC). This article explores the relationship between ferroptosis-related gene (FRG) expression and prognosis in EC patients. One hundred thirty-five FRGs were obtained by mining the literature, retrieving GeneCards and analyzing 552 malignant uterine corpus endometrial carcinoma (UCEC) samples, which were randomly assigned to training and testing groups (1:1 ratio), and 23 normal samples from The Cancer Genome Atlas (TCGA).
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ONCOLOGY REPORTS 37: 3253-3260, 2017 Association of long-chain acyl-coenzyme A synthetase 5 expression in human breast cancer by estrogen receptor status and its clinical significance MEng-CHI YEn1*, JUNG-YU KAN2,3*, CHIA-Jung HSIEH4,5, PO-LIn KuO2, MIng-FEng HOu2,3 and YA-LIng HSu4 1Department of Emergency Medicine, Kaohsiung Medical university Hospital, Kaohsiung 807; 2graduate Institute of Clinical Medicine, College of Medicine, Kaohsiung Medical university, Kaohsiung 807; 3Department of Breast Surgery, Kaohsiung Medical university Hospital, Kaohsiung 807; 4graduate Institute of Medicine, College of Medicine, Kaohsiung Medical university, Kaohsiung 807; 5Department of Chinese Medicine, Kaohsiung Medical university Hospital, Kaohsiung 807, Taiwan, R.O.C. Received February 6, 2017; Accepted April 21, 2017 DOI: 10.3892/or.2017.5610 Abstract. The lipid metabolic enzymes are considered suggest that ACSL1, ACSL4 and ACSL5 expression is regu- candidate therapeutic targets for breast cancer. Long-chain lated by ER signaling pathways and ACSL5 is a potential novel acyl-coenzyme A (CoA) synthase (ACSL) is one of lipid biomarker for predicting prognosis of breast cancer patients. metabolic enzymes and converts free-fatty acid to fatty acid-CoA. Five ACSL isoforms including ACSL1, ACSL3, Introduction ACSL4, ACSL5 and ACSL6 are identified in human. High ACSL4 expression has been observed in aggressive breast Dysregulation of metabolic pathways, including regulation cancer phenotype. However, the role of other isoforms is still of glucose transporter, tricarboxylic acid cycle (TCA cycle), little-known. We therefore, analyzed the expression of ACSL pentose phosphate pathway and mitochondria respiratory isoforms in each subtype of breast cancer within METABRIC chain are observed in many types of cancers (1).
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