ArticleCell stress & chaperones2017
SG2NA is a regulator of endoplasmic reticulum (ER) homeostasis as its depletion leads to ER stress.
Article in Cell stress & chaperones, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- TRAF3IP3 Induces ER Stress-Mediated Apoptosis with Protective Autophagy to Inhibit Lung Adenocarcinoma Proliferation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Remodeling of the cardiac striatin interactome and its dynamics in the diabetic heart.Scientific reports · 2025Article
- STRIPAK, a fundamental signaling hub of eukaryotic development.Microbiology and molecular biology reviews : MMBR · 2024Review
- Review
- The profile of expression of the scaffold protein SG2NA(s) differs between cancer types and its interactome in normal vis-a-vis breast tumor tissues suggests its wide roles in regulating multiple cellular pathways.Molecular and cellular biochemistry · 2022Article
- Ectopic expression of 35 kDa and knocking down of 78 kDa SG2NAs induce cytoskeletal reorganization, alter membrane sialylation, and modulate the markers of EMT.Molecular and cellular biochemistry · 2021Article
- Striatin Is Required for Hearing and Affects Inner Hair Cells and Ribbon Synapses.Frontiers in cell and developmental biology · 2020Article
- WD40 Repeat Proteins: Signalling Scaffold with Diverse Functions.The protein journal · 2018Review
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Authors and funding
6 authors.
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No grant is acknowledged in the PubMed record.
Abstract
SG2NA belongs to a three-member striatin subfamily of WD40 repeat superfamily of proteins. It has multiple protein-protein interaction domains involved in assembling supramolecular signaling complexes. Earlier, we had demonstrated that there are at least five variants of SG2NA generated by alternative splicing, intron retention, and RNA editing. Such versatile and dynamic mode of regulation implicates it in tissue development. In order to shed light on its role in cell physiology, total proteome analysis was performed in NIH3T3 cells depleted of 78 kDa SG2NA, the only isoform expressing therein. A number of ER stress markers were among those modulated after knockdown of SG2NA. In cells treated with the ER stressors thapsigargin and tunicamycin, expression of SG2NA was increased at both mRNA and protein levels. The increased level of SG2NA was primarily in the mitochondria and the microsomes. A mouse injected with thapsigargin also had an increase in SG2NA in the liver but not in the brain. Cell cycle analysis suggested that while loss of SG2NA reduces the level of cyclin D1 and retains a population of cells in the G1 phase, concurrent ER stress facilitates their exit from G1 and traverse through subsequent phases with concomitant cell death. Thus, SG2NA is a component of intrinsic regulatory pathways that maintains ER homeostasis.
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