ArticleMolecular and cellular biology1998
Structure-function analysis of Qk1: a lethal point mutation in mouse quaking prevents homodimerization.
Article in Molecular and cellular biology, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.
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Who cites it
64 citing papers in PubMed, 123 citations in OpenAlex.
- RNA-Binding Proteins: Modulators of Canonical Wnt Signaling Pathway.International journal of molecular sciences · 2025Review
- RNA-binding protein quaking: a multifunctional regulator in tumour progression.Annals of medicine · 2025Review
- Diverse roles of quaking in endothelial cell biology.Angiogenesis · 2025Review
- Dysregulation of zebrin-II cell subtypes in the cerebellum is a shared feature across polyglutamine ataxia mouse models and patients.Science translational medicine · 2024Article
- The multifaceted role of quaking protein in neuropsychiatric disorders and tumor progression.Frontiers in neuroscience · 2024Review
- Functions of METTL1/WDR4 and QKI as m7G modification - related enzymes in digestive diseases.Frontiers in pharmacology · 2024Review
- Purkinje-Enriched snRNA-seq in SCA7 Cerebellum Reveals Zebrin Identity Loss as a Central Feature of Polyglutamine Ataxias.bioRxiv : the preprint server for biology · 2023Article
- The Quaking RNA-binding proteins as regulators of cell differentiation.Wiley interdisciplinary reviews. RNA · 2022Review
- The Long Non-Coding RNACells · 2022Review
- Muscle stem cell polarity requires QKI-mediated alternative splicing of Integrin Alpha-7 (Itga7).Life science alliance · 2022Article
- Regulatory RNAs, microRNA, long-non coding RNA and circular RNA roles in colorectal cancer stem cells.World journal of gastrointestinal oncology · 2022Review
- Gld2 activity and RNA specificity is dynamically regulated by phosphorylation and interaction with QKI-7.RNA biology · 2021Article
- Loss of Quaking RNA binding protein disrupts the expression of genes associated with astrocyte maturation in mouse brain.Nature communications · 2021Article
- QKI is a critical pre-mRNA alternative splicing regulator of cardiac myofibrillogenesis and contractile function.Nature communications · 2021Article
- The Emerging Roles of the RNA Binding Protein QKI in Cardiovascular Development and Function.Frontiers in cell and developmental biology · 2021Review
- Targeting the RNA-Binding ProteinEpigenomes · 2020Article
- Identification of Novel Binding Partners for Transcription Factor Emx2.The protein journal · 2019Article
- Molecular Characterization of the RNA-Binding Protein Quaking-a inFrontiers in physiology · 2018Article
- CRAF gene fusions in pediatric low-grade gliomas define a distinct drug response based on dimerization profiles.Oncogene · 2017Article
- Roles of microRNAs and RNA-Binding Proteins in the Regulation of Colorectal Cancer Stem Cells.Cancers · 2017Review
4 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Qk1 is a member of the KH domain family of proteins that includes Sam68, GRP33, GLD-1, SF1, and Who/How. These family members are RNA binding proteins that contain an extended KH domain embedded in a larger domain called the GSG (for GRP33-Sam68-GLD-1) domain. An ethylnitrosourea-induced point mutation in the Qk1 GSG domain alters glutamic acid 48 to a glycine and is known to be embryonically lethal in mice. The function of Qk1 and the GSG domain as well as the reason for the lethality are unknown. Here we demonstrate that the Qk1 GSG domain mediates RNA binding and Qk1 self-association. By using in situ chemical cross-linking studies, we showed that the Qk1 proteins exist as homodimers in vivo. The Qk1 self-association region was mapped to amino acids 18 to 57, a region predicted to form coiled coils. Alteration of glutamic acid 48 to glycine (EG) in the Qk1 GSG domain (producing protein Qk1:EG) abolishes self-association but has no effect on the RNA binding activity. The expression of Qk1 or Qk1:EG in NIH 3T3 cells induces cell death by apoptosis. Approximately 90% of the remaining transfected cells are apoptotic 48 h after transfection. Qk1:EG was consistently more potent at inducing apoptosis than was wild-type Qk1. These results suggest that the mouse quaking lethality (EG) occurs due to the absence of Qk1 self-association mediated by the GSG domain.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.