SMG-1 Antibody [L4N6] | Primary Antibodies

Application: Reactivity: Human, Monkey

Lane 1: U2OS, Lane 2: 293, Lane 3: MCF7

Usage Information

Dilution
WB1:1000 IP1:50

Application
WB, IP

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
410 kDa

Datasheet & SDS

Biological Description

Specificity
SMG-1 Antibody [L4N6] detects endogenous levels of total SMG-1 protein.

Clone
L4N6

Synonym(s)
Serine/threonine-protein kinase SMG1; SMG-1; hSMG-1; Lambda/iota protein kinase C-interacting protein; Lambda-interacting protein; Nonsense mediated mRNA decay-associated PI3K-related kinase SMG1; SMG1; ATX; KIAA0421; LIP

Background
SMG‑1 is a large serine/threonine kinase and a member of the phosphoinositide 3‑kinase‑related kinase (PIKK) family, which includes ATM, ATR, mTOR, DNA‑PKcs, and TRRAP, and it is widely expressed in mammalian cells where it functions as a core regulator of mRNA quality control and stress‑responsive signaling. SMG‑1 forms a stable complex with SMG‑8 and SMG‑9, and this assembly targets the RNA‑binding protein UPF1 (hUpf1) for phosphorylation following recognition of premature termination codons on spliced mRNAs, thereby triggering nonsense‑mediated mRNA decay (NMD) and preventing the accumulation of truncated, nonfunctional or aberrant proteins. SMG‑1 phosphorylates p53 and other substrates in response to DNA damage and genotoxic stress, and it contributes to cell‑cycle control by modulating the G1/S checkpoint through both p53‑dependent and p53‑independent mechanisms, including regulation of Cdc25A and suppression of CDK2 activity. SMG‑1 activity intersects with DNA‑damage and survival pathways, and exhibits the potential to protect cells from extrinsically induced apoptosis by influencing cell‑death‑receptor signaling and by stabilizing anti‑apoptotic regulators such as c‑FLIP, which dampens caspase‑8 activation in response to TNFα and Smac‑mimetic compounds. Loss or inhibition of SMG‑1 increases sensitivity to DNA‑damaging agents and to extrinsic apoptotic stimuli, and reduced SMG‑1 expression or function has been associated with impaired NMD, altered cell‑cycle progression, and either tumor‑suppressive or context‑dependent oncogenic phenotypes in different cancers.

Background

SMG‑1 is a large serine/threonine kinase and a member of the phosphoinositide 3‑kinase‑related kinase (PIKK) family, which includes ATM, ATR, mTOR, DNA‑PKcs, and TRRAP, and it is widely expressed in mammalian cells where it functions as a core regulator of mRNA quality control and stress‑responsive signaling. SMG‑1 forms a stable complex with SMG‑8 and SMG‑9, and this assembly targets the RNA‑binding protein UPF1 (hUpf1) for phosphorylation following recognition of premature termination codons on spliced mRNAs, thereby triggering nonsense‑mediated mRNA decay (NMD) and preventing the accumulation of truncated, nonfunctional or aberrant proteins. SMG‑1 phosphorylates p53 and other substrates in response to DNA damage and genotoxic stress, and it contributes to cell‑cycle control by modulating the G1/S checkpoint through both p53‑dependent and p53‑independent mechanisms, including regulation of Cdc25A and suppression of CDK2 activity. SMG‑1 activity intersects with DNA‑damage and survival pathways, and exhibits the potential to protect cells from extrinsically induced apoptosis by influencing cell‑death‑receptor signaling and by stabilizing anti‑apoptotic regulators such as c‑FLIP, which dampens caspase‑8 activation in response to TNFα and Smac‑mimetic compounds. Loss or inhibition of SMG‑1 increases sensitivity to DNA‑damaging agents and to extrinsic apoptotic stimuli, and reduced SMG‑1 expression or function has been associated with impaired NMD, altered cell‑cycle progression, and either tumor‑suppressive or context‑dependent oncogenic phenotypes in different cancers.

References
https://pubmed.ncbi.nlm.nih.gov/16289965/ https://pubmed.ncbi.nlm.nih.gov/24107632/

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%