Glutaminase1/GLS1 Antibody [A10K11]

Application: Reactivity: Human, Monkey

Lane 1: ACHN

Usage Information

Dilution
WB1:1000 IP1:200 IHC1:200-1:800

Application
WB, IP, IHC

Reactivity
Human, Monkey

Source
Rabbit Monoclonal Antibody

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
55-65 kDa

Datasheet & SDS

Biological Description

Specificity
Glutaminase1/GLS1 Antibody [A10K11] detects endogenous levels of total Glutaminase1/GLS1 protein.

Clone
A10K11

Synonym(s)
Glutaminase kidney isoform, mitochondrial; GLS; K-glutaminase; L-glutamine amidohydrolase; GLS1; KIAA0838

Background
Glutaminase‑1 (GLS1) is a mitochondrial phosphate‑dependent amidotransferase and the major kidney‑type isoform of glutaminase that catalyzes the hydrolysis of glutamine to glutamate, the first and rate‑limiting step in glutaminolysis. GLS1 is expressed in multiple tissues, including the kidney and metabolically active cancer cells, where it channels glutamine‑derived nitrogen and carbon into the tricarboxylic acid cycle, nucleotide synthesis, and glutathione production. GLS1‑mediated glutamate generation supports both energy production and redox homeostasis by supplying precursors for NADPH and glutathione synthesis in proliferating cells, and GLS1 activity is upregulated in contexts such as post‑implantation bone‑marrow‑derived cells preconditioned to hypoxia, where it enhances survival under ischemic stress. In KRAS‑mutant lung adenocarcinoma, tumors with co‑occurring LKB1 loss and KEAP1/NRF2 alterations show enhanced glutamine dependence and increased GLS1‑driven glutaminolysis, which sustains their growth and sensitizes them to GLS1 inhibition. By integrating glutamine‑ and glucose‑metabolism pathways, GLS1 helps coordinate glycolysis, lactate production, and glutamine‑derived anaplerosis, and its inhibition reduces glucose uptake and lactate output in some carcinoma models.

Background

Glutaminase‑1 (GLS1) is a mitochondrial phosphate‑dependent amidotransferase and the major kidney‑type isoform of glutaminase that catalyzes the hydrolysis of glutamine to glutamate, the first and rate‑limiting step in glutaminolysis. GLS1 is expressed in multiple tissues, including the kidney and metabolically active cancer cells, where it channels glutamine‑derived nitrogen and carbon into the tricarboxylic acid cycle, nucleotide synthesis, and glutathione production. GLS1‑mediated glutamate generation supports both energy production and redox homeostasis by supplying precursors for NADPH and glutathione synthesis in proliferating cells, and GLS1 activity is upregulated in contexts such as post‑implantation bone‑marrow‑derived cells preconditioned to hypoxia, where it enhances survival under ischemic stress. In KRAS‑mutant lung adenocarcinoma, tumors with co‑occurring LKB1 loss and KEAP1/NRF2 alterations show enhanced glutamine dependence and increased GLS1‑driven glutaminolysis, which sustains their growth and sensitizes them to GLS1 inhibition. By integrating glutamine‑ and glucose‑metabolism pathways, GLS1 helps coordinate glycolysis, lactate production, and glutamine‑derived anaplerosis, and its inhibition reduces glucose uptake and lactate output in some carcinoma models.

References
https://pubmed.ncbi.nlm.nih.gov/29578539/ https://pubmed.ncbi.nlm.nih.gov/31040157/

Reference Table for Selecting PVDF Membrane Pore Size Specifications

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%