NPRL2 Antibody [L19L7] | Primary Antibodies

Application: Reactivity: Human, Mouse, Rat, Monkey

Usage Information

Dilution
WB1:1000 IP1:50

Application
WB, IP

Reactivity
Human, Mouse, Rat, 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
41 kDa

Positive Control	LNCaP cells; DLD-1 cells; MCF-7 cells; IGROV-1 cells
Negative Control

Datasheet & SDS

Biological Description

Specificity
NPRL2 Antibody [L19L7] detects endogenous levels of total NPRL2 protein.

Clone
L19L7

Synonym(s)
GATOR1 complex protein NPRL2; Gene 21 protein 1 publication (G21 protein); Nitrogen permease regulator 2-like protein (NPR2-like protein); Tumor suppressor candidate 4; NPRL2; TUSC4

Background
NPRL2 (also known as TUSC4) is a core component of the GATOR1 complex (with DEPDC5 and NPRL3), functioning as a negative regulator of mTORC1 signaling by acting as a GAP (GTPase-activating protein) for RagA/B GTPases, thereby inhibiting amino acid-induced mTORC1 translocation to lysosomes under nutrient limitation to suppress anabolic processes like protein synthesis. NPRL2 features an N-terminal Longin domain (residues ~1–180) for Rag GTPase binding and GAP activity, a central helical domain facilitating DEPDC5/NPRL3 heterodimerization, and a C-terminal region enabling lysosomal membrane association and selective Raptor interaction; key residues in the Longin domain (e.g., conserved Arg/Lys motifs, notably Arg78) catalyze GTP hydrolysis on RagA GDP/RagD GTP heterodimers. During amino acid sufficiency NPRL2 paradoxically interacts with Raptor to fine-tune mTORC1 activation via a "seesaw" mechanism, releasing Rag inhibition while preventing overactivation, while amino acid scarcity shifts NPRL2-Rag binding to robustly suppress mTORC1, maintaining metabolic homeostasis. NPRL2 overexpression inhibits cell proliferation by sustaining BRCA1 stability and inducing ROS via NOX2/mitochondrial dysfunction, triggering DNA damage responses and apoptosis in p53-proficient cells. NPRL2 ensures neurometabolic balance (e.g., regulating sodium channel expression in neurons), prevents excessive growth under stress, and acts as a tumor suppressor limiting mTORC1-driven oncogenesis. Pathogenic germline mutations cause familial focal epilepsies and mTORopathies (e.g., cortical dysplasia) due to hyperactive mTORC1, while somatic loss promotes tumorigenesis.

Background

NPRL2 (also known as TUSC4) is a core component of the GATOR1 complex (with DEPDC5 and NPRL3), functioning as a negative regulator of mTORC1 signaling by acting as a GAP (GTPase-activating protein) for RagA/B GTPases, thereby inhibiting amino acid-induced mTORC1 translocation to lysosomes under nutrient limitation to suppress anabolic processes like protein synthesis. NPRL2 features an N-terminal Longin domain (residues ~1–180) for Rag GTPase binding and GAP activity, a central helical domain facilitating DEPDC5/NPRL3 heterodimerization, and a C-terminal region enabling lysosomal membrane association and selective Raptor interaction; key residues in the Longin domain (e.g., conserved Arg/Lys motifs, notably Arg78) catalyze GTP hydrolysis on RagA GDP/RagD GTP heterodimers. During amino acid sufficiency NPRL2 paradoxically interacts with Raptor to fine-tune mTORC1 activation via a "seesaw" mechanism, releasing Rag inhibition while preventing overactivation, while amino acid scarcity shifts NPRL2-Rag binding to robustly suppress mTORC1, maintaining metabolic homeostasis. NPRL2 overexpression inhibits cell proliferation by sustaining BRCA1 stability and inducing ROS via NOX2/mitochondrial dysfunction, triggering DNA damage responses and apoptosis in p53-proficient cells. NPRL2 ensures neurometabolic balance (e.g., regulating sodium channel expression in neurons), prevents excessive growth under stress, and acts as a tumor suppressor limiting mTORC1-driven oncogenesis. Pathogenic germline mutations cause familial focal epilepsies and mTORopathies (e.g., cortical dysplasia) due to hyperactive mTORC1, while somatic loss promotes tumorigenesis.

References
https://pubmed.ncbi.nlm.nih.gov/38963491/ https://pubmed.ncbi.nlm.nih.gov/35165201/

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%