Evidence map›Paper›PMID 16227613›Full record

ArticleMolecular and cellular biology2005

Phosphotyrosine 1062 is critical for the in vivo activity of the Ret9 receptor tyrosine kinase isoform.

Adrianne Wong, Silvia Bogni, Pille Kotka, Esther de Graaff, Vivette D'Agati, Frank Costantini, Vassilis Pachnis

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
2.6field-weighted citation impact, top 10% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

47 citing papers in PubMed, 89 citations in OpenAlex.

  1. CCDC6-RET fusion protein regulates Ras/MAPK signaling through the fusion- GRB2-SHC1 signal niche.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  2. Review
  3. TheAIMS neuroscience · 2022
    Review
  4. Article
  5. RET receptor signaling: Function in development, metabolic disease, and cancer.Proceedings of the Japan Academy. Series B, Physical and biological sciences · 2022
    Review
  6. Multiple Roles of Ret Signalling During Enteric Neurogenesis.Frontiers in molecular neuroscience · 2022
    Article
  7. Article
  8. Review
  9. Article
  10. MAPK/ERK Signaling in Regulation of Renal Differentiation.International journal of molecular sciences · 2019
    Review
  11. Review
  12. Reciprocal Spatiotemporally Controlled Apoptosis Regulates Wolffian Duct Cloaca Fusion.Journal of the American Society of Nephrology : JASN · 2018
    Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. To bud or not to bud: the RET perspective in CAKUT.Pediatric nephrology (Berlin, Germany) · 2014
    Review
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 1 institution in 1 country.

Adrianne WongDivision of Molecular Neurobiology, MRC National Institute for Medical Research, The Ridgeway, Mill Hill, London NW7 1AA, United Kingdom.
Silvia Bogni
Pille Kotka
Esther de Graaff
Vivette D'Agati
Frank Costantini
Vassilis Pachnis
Columbia University Irving Medical Center · US

Funding

THE DETERMINANTS OF MUTATIONP01CA023767 · NCI · COLUMBIA UNIV NEW YORK MORNINGSIDE · PI AXEL, RICHARD · 1985 to 2008
$8.3M
Medical Research Council MC_U117537087NCI NIH HHS CA 23767NCI NIH HHS P01 CA023767Telethon 438/B
6 · The paper itself

Abstract

The receptor tyrosine kinase Ret plays a critical role in the development of the mammalian excretory and enteric nervous systems. Differential splicing of the primary Ret transcript results in the generation of two main isoforms, Ret9 and Ret51, whose C-terminal amino acid tails diverge after tyrosine (Y) 1062. Monoisoformic mice expressing only Ret9 develop normally and are healthy and fertile. In contrast, animals expressing only Ret51 have aganglionosis of the distal gut and hypoplastic kidneys. By generating monoisoformic mice in which Y1062 of Ret9 has been mutated to phenylalanine, we demonstrate that this amino acid has a critical role in Ret9 signaling that is necessary for the development of the kidneys and the enteric nervous system. These findings argue that the distinct activities of Ret9 and Ret51 result from the differential regulation of Y1062 by C-terminal flanking sequences. However, a mutation which places Y1062 of Ret51 in a Ret9 context improves only marginally the ability of Ret51 to support renal and enteric nervous system development. Finally, monoisoformic mice expressing a variant of Ret9 in which a C-terminal PDZ-binding motif was mutated develop normally and are healthy. Our studies identify Y1062 as a critical regulator of Ret9 signaling and suggest that Ret51-specific motifs are likely to inhibit the activity of this isoform.

Indexed as

Alternative SplicingAmino Acid MotifsAnimalsAnimals, NewbornEnteric Nervous SystemHumansIsoenzymesKidneyMiceMice, Mutant StrainsMutationPhosphotyrosineProto-Oncogene Proteins c-retSignal TransductionIsoenzymesPhosphotyrosineProto-Oncogene Proteins c-retRET protein, human

Identifiers

PMID16227613
PMCPMC1265823
OpenAlexW2104281780

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.