Cited by 38RNA Research and SplicingDevelopmental Biology and Gene RegulationCancer-related molecular mechanisms research

The Quaking family of RNA-binding proteins: Coordinators of the cell cycle and differentiation

Open access
Biedermann, Bjoern, Hotz, Hans-Rudolf, Ciosk, Rafal·2010·Cell Cycle

Abstract

Transcriptional and epigenetic control of gene expression is critical for cell fate specification, commitment and terminal differentiation during development. However, also regulatory RNAs and RNA-binding proteins have emerged as critical developmental regulators. They control various aspects of mRNA metabolism such as stability, translation, and localization, and similar to some transcriptional regulators, such as PAX5 and MYC, they can affect gene expression on a massive scale. Consistently, defects in many mRNA regulators have been implicated in a number of human disorders, including cancer. Quaking-related (QR) proteins are conserved RNA-binding proteins of the STAR (signal transduction and activation of RNA) family. QR proteins regulate expression of diverse mRNA targets by various mechanisms, play essential roles in a whole host of developmental decisions, and function as tumor suppressors. This review discusses several best-studied members of the QR family, their developmental functions, molecular mechanisms, representative mRNA targets, and their intriguing ability to coordinately control the cell cycle and a wide range of differentiation pathways.

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.4161/cc.9.10.11533

Cites

47 of 47 references verified0 citation errors · 0 not checkable

Statistics

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Cites

Flagged first, then by citations

3 of the 50 references couldn’t be matched to a known paper.

Research works printed but not linked: 20

  1. Lee MH, Schedl T. Translation repression by GLD-1 protects its mRNA targets from nonsense-mediated mRNA decay in C. elegans. Genes Dev 2004; 18:1047- 59.
  2. Hsu V, Zobel CL, Lambie EJ, Schedl T, Kornfeld K. Caenorhabditis elegans lin-45 raf is essential for larval viability, fertility and the induction of vulval cell fates. Genetics 2002; 160:481-92.
  3. Mootz D, Ho DM, Hunter CP. The STAR/Maxi-KH domain protein GLD-1 mediates a developmental switch in the translational control of C. elegans PAL-1. Development 2004; 131:3263-72.
  4. Zaffran S, Astier M, Gratecos D, Semeriva M. The held out wings (how) Drosophila gene encodes a putative RNA-binding protein involved in the control of muscular and cardiac activity. Development 1997; 124:2087-98.
  5. Baehrecke EH. Who encodes a KH RNA bind- ing protein that functions in muscle development. Development 1997; 124:1323-32.
  6. Israeli D, Nir R, Volk T. Dissection of the target speci- ficity of the RNA-binding protein HOW reveals dpp mRNA as a novel HOW target. Development 2007; 134:2107-14.
  7. Toledano-Katchalski H, Nir R, Volohonsky G, Volk T. Post-transcriptional repression of the Drosophila midkine and pleiotrophin homolog miple by HOW is essential for correct mesoderm spreading. Development 2007; 134:3473-81.
  8. Lo PC, Frasch M. A novel KH-domain protein medi- ates cell adhesion processes in Drosophila. Dev Biol 1997; 190:241-56.
  9. Noveroske JK, Lai L, Gaussin V, Northrop JL, Nakamura H, Hirschi KK, Justice MJ. Quaking is essential for blood vessel development. Genesis 2002; 32:218-30.
  10. Li Z, Takakura N, Oike Y, Imanaka T, Araki K, Suda T, et al. Defective smooth muscle development in qkI- deficient mice. Dev Growth Differ 2003; 45:449-62.
  11. Wu JI, Reed RB, Grabowski PJ, Artzt K. Function of quaking in myelination: regulation of alternative splic- ing. Proc Natl Acad Sci USA 2002; 99:4233-8.
  12. Li Z, Zhang Y, Li D, Feng Y. Destabilization and mislocalization of myelin basic protein mRNAs in quaking dysmyelination lacking the QKI RNA-binding proteins. J Neurosci 2000; 20:4944-53.
  13. Zhao L, Tian D, Xia M, Macklin WB, Feng Y. Rescuing qkV dysmyelination by a single isoform of the selective RNA-binding protein QKI. J Neurosci 2006; 26:11278-86.
  14. Lee MH, Schedl T. Identification of in vivo mRNA targets of GLD-1, a maxi-KH motif containing protein required for C. elegans germ cell development. Genes Dev 2001; 15:2408-20.
  15. Marin VA, Evans TC. Translational repression of a C. elegans Notch mRNA by the STAR/KH domain pro- tein GLD-1. Development 2003; 130:2623-32.
  16. Chen T, Richard S. Structure-function analysis of Qk1: a lethal point mutation in mouse quaking prevents homodimerization. Mol Cell Biol 1998; 18:4863-71.
  17. Cox RD, Hugill A, Shedlovsky A, Noveroske JK, Best S, Justice MJ, et al. Contrasting effects of ENU induced embryonic lethal mutations of the quaking gene. Genomics 1999; 57:333-41.
  18. Bushati N, Cohen SM. microRNA functions. Annu Rev Cell Dev Biol 2007; 23:175-205.
  19. Hardy RJ. QKI expression is regulated during neuron- glial cell fate decisions. J Neurosci Res 1998; 54:46- 57.
  20. Volohonsky G, Edenfeld G, Klambt C, Volk T. Muscle- dependent maturation of tendon cells is induced by post-transcriptional regulation of stripeA. Development 2007; 134:347-56.

Cited by

Sorted by citations

Authors
Biedermann, B., Hotz, H.-R., & Ciosk, R.
Affiliations
Friedrich Miescher Institute (CH)
Corresponding author
Ciosk, Rafal
Venue
Cell Cycle
Published
2010-05-15
Volume
9
Issue
10
Pages
1929-1933
ISSN
  • 1538-4101 (ISSN-L)
  • 1551-4005
OpenAlex
W1996787489
Cited by
37
References
50
Citations by year
2023: 2 · 2022: 1 · 2021: 1 · 2020: 2 · 2019: 3 · 2018: 2 · 2017: 4 · 2016: 4 · 2015: 2 · 2014: 4 · 2013: 7 · 2012: 4
FWCI
0.34
Type
journal article
Language
en
Open access
Licence
cc-by-nc
Locations
  • Cell Cycle (publishedVersion, cc-by-nc)
  • PubMed (publishedVersion)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › RNA Research and Splicing
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Developmental Biology and Gene Regulation
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer-related molecular mechanisms research
Keywords
RNA-binding proteins, cell cycle regulation, cell differentiation, developmental regulation, mRNA stability, mRNA localization, translational regulation, tumor suppressor, cancer, epigenetic regulation, gene expression regulation
MeSH terms
Animals, Cell Cycle, Cell Differentiation, Humans, Models, Biological, Phylogeny, RNA-Binding Proteins

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review