ACSL1 Antibody [D13B22]

Catalog No.: F4805

Application: Reactivity: Human

Lane 1: Raji

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代表番号: 045-509-1970|電子メール：sales@selleck.co.jp

使用情報

Dilution
WB1:1000 - 1:10000 IHC1:100 - 1:250

Application
WB, IHC

Source
Rabbit Monoclonal Antibody

Reactivity
Human

Storage Buffer
PBS, pH 7.2+50% Glycerol+0.05% BSA+0.01% NaN3

Storage (from the date of receipt)
-20°C (avoid freeze-thaw cycles), 2 years

Predicted MW Observed MW
78 kDa 75 kDa
^*なぜ予測分子量と実際の分子量が異なるのか？下記の原因により、実際の分子量が予測と異なる：タンパク質の翻訳後修飾（リン酸化/糖鎖付加），スプライシングバリアント，イソフォーム，相対的な電荷，ポリマー。

Datasheet & SDS

生物学的記述

Specificity
ACSL1 Antibody [D13B22] detects endogenous levels of total ACSL1 protein.

Clone
D13B22

Synonym(s)
FACL1; FACL2; LACS; LACS1; LACS2; ACSL1; Long-chain-fatty-acid--CoA ligase 1; Acyl-CoA synthetase 1; Arachidonate--CoA ligase; Long-chain acyl-CoA synthetase 1; Long-chain acyl-CoA synthetase 2; Long-chain fatty acid-CoA ligase 2; Palmitoyl-CoA ligase 1; Palmitoyl-CoA ligase 2; Phytanate--CoA ligase; ACS1; LACS 1; LACS 2

Background
Acyl-CoA synthetase long-chain family member 1 (ACSL1) is a pivotal enzyme in lipid metabolism, responsible for activating long-chain fatty acids (C12–C20) by catalyzing their conversion into fatty acyl-CoA thioesters in an ATP- and CoA-dependent reaction. This activation is essential for channeling fatty acids into downstream metabolic pathways, including mitochondrial β-oxidation for energy production, complex lipid synthesis (such as triglycerides and phospholipids), and lipid signaling, thereby maintaining cellular energy homeostasis and lipid balance. ACSL1 is an amino-acid protein with a large N-terminal catalytic domain and a smaller C-terminal domain; its architecture includes a conserved AMP-binding region with characteristic motifs (A3, A5, A8, A10), a fatty acid-binding pocket, and Walker A/B-like motifs that facilitate its two-step “ping-pong” mechanism, first forming an acyl-AMP intermediate, then transferring the acyl group to CoA. ACSL1 localizes to the endoplasmic reticulum, mitochondria, and peroxisomes, where it interacts with carnitine palmitoyltransferase 1 (CPT1) to direct acyl-CoAs toward β-oxidation or with lipid droplets to promote triglyceride synthesis, thus partitioning specific fatty acids (oleate or palmitate) into metabolic fates according to cellular energy needs. Its expression is transcriptionally regulated by PPARα and SREBP-1c in response to nutrient and hormonal cues, supporting metabolic flexibility in tissues such as liver, heart, and adipose tissue. Dysregulation of ACSL1, through overexpression or genetic variation, contributes to hepatic steatosis, ER stress, and the development of insulin resistance and atherosclerosis, while knockdown or loss-of-function models reveal its critical role in obesity, cardiovascular disease, and cancer lipid metabolism.

Background

Acyl-CoA synthetase long-chain family member 1 (ACSL1) is a pivotal enzyme in lipid metabolism, responsible for activating long-chain fatty acids (C12–C20) by catalyzing their conversion into fatty acyl-CoA thioesters in an ATP- and CoA-dependent reaction. This activation is essential for channeling fatty acids into downstream metabolic pathways, including mitochondrial β-oxidation for energy production, complex lipid synthesis (such as triglycerides and phospholipids), and lipid signaling, thereby maintaining cellular energy homeostasis and lipid balance. ACSL1 is an amino-acid protein with a large N-terminal catalytic domain and a smaller C-terminal domain; its architecture includes a conserved AMP-binding region with characteristic motifs (A3, A5, A8, A10), a fatty acid-binding pocket, and Walker A/B-like motifs that facilitate its two-step “ping-pong” mechanism, first forming an acyl-AMP intermediate, then transferring the acyl group to CoA. ACSL1 localizes to the endoplasmic reticulum, mitochondria, and peroxisomes, where it interacts with carnitine palmitoyltransferase 1 (CPT1) to direct acyl-CoAs toward β-oxidation or with lipid droplets to promote triglyceride synthesis, thus partitioning specific fatty acids (oleate or palmitate) into metabolic fates according to cellular energy needs. Its expression is transcriptionally regulated by PPARα and SREBP-1c in response to nutrient and hormonal cues, supporting metabolic flexibility in tissues such as liver, heart, and adipose tissue. Dysregulation of ACSL1, through overexpression or genetic variation, contributes to hepatic steatosis, ER stress, and the development of insulin resistance and atherosclerosis, while knockdown or loss-of-function models reveal its critical role in obesity, cardiovascular disease, and cancer lipid metabolism.

References
[1] Deng X, et al. Mol Biomed. 2025 Nov 25;6(1):117. [2] Yan S, et al. World J Gastroenterol. 2015 Mar 28;21(12):3492-8.

PVDFメンブレン孔径参考表

Protein Size (kDa)	PVDF Transfer Membrane Pore Size (μm)
< 10	0.22
10-20	0.22
20-30	0.45
30-45	0.45
45-70	0.45
80-100	0.45
100-140	0.45
> 140	0.45

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Protein Size (kDa)	Separating Gel Percentage
4-40	20%
12-45	15%
10-70	12.5%
15-100	10%
25-100	8%
60-210	5%