Evidence map›Paper›PMID 29079424›Full record

ReviewDevelopmental biology2019

Feedback regulation of RTK signaling in development.

Cynthia L Neben, Megan Lo, Natalia Jura, Ophir D Klein

Abstract readReview
In one paragraph

Review in Developmental biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

52 citing papers in PubMed, 86 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Downstream branches of receptor tyrosine kinase signaling act interdependently to shape the face.Developmental dynamics : an official publication of the American Association of Anatomists · 2025
    Article
  7. Article
  8. Review
  9. Article
  10. bioRxiv : the preprint server for biology · 2025
    Article
  11. Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Phenotypic consequences of logarithmic signaling in MAPK stress response.bioRxiv : the preprint server for biology · 2023
    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

4 authors at 1 institution in 1 country.

Cynthia L NebenDepartment of Orofacial Sciences and Program in Craniofacial Biology, University of California, San Francisco, San Francisco 94143, USA.
Megan LoDepartment of Orofacial Sciences and Program in Craniofacial Biology, University of California, San Francisco, San Francisco 94143, USA; Cardiovascular Research Institute, University of California, San Francisco, San Francisco, CA, USA.
Natalia JuraCardiovascular Research Institute, University of California, San Francisco, San Francisco, CA, USA; Department of Cellular and Molecular Pharmacology, University of California, San Francisco, San Francisco, CA, USA. Electronic address: natalia.jura@ucsf.edu.
Ophir D KleinDepartment of Orofacial Sciences and Program in Craniofacial Biology, University of California, San Francisco, San Francisco 94143, USA; Department of Pediatrics and Institute for Human Genetics, University of California, San Francisco, San Francisco 94143, USA. Electronic address: ophir.klein@ucsf.edu.
University of California, San Francisco · US

Funding

NRSA Training CoreTL1TR001871 · NCATS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI KANAYA, ALKA M., SOMSOUK, MA · 2016 to 2025
$10.1M
Harnessing natural stem cell-based strategies for mammalian dental renewalR35DE026602 · NIDCR · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI KLEIN, OPHIR D · 2016 to 2023
$8.0M
PHARMACEUTICAL SCIENCES AND PHARMACOGENOMICST32GM007175 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI AHITUV, NADAV, KROETZ, DEANNA L · 1985 to 2021
$7.1M
Structural and Functional Studies of HER Receptor Tyrosine KinasesR01GM109176 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI JURA, NATALIA · 2014 to 2018
$1.8M
NCATS NIH HHS TL1 TR001871NIDCR NIH HHS R35 DE026602NIGMS NIH HHS R01 GM109176NIGMS NIH HHS T32 GM007175
6 · The paper itself

Abstract

Precise regulation of the amplitude and duration of receptor tyrosine kinase (RTK) signaling is critical for the execution of cellular programs and behaviors. Understanding these control mechanisms has important implications for the field of developmental biology, and in recent years, the question of how augmentation or attenuation of RTK signaling via feedback loops modulates development has become of increasing interest. RTK feedback regulation is also important for human disease research; for example, germline mutations in genes that encode RTK signaling pathway components cause numerous human congenital syndromes, and somatic alterations contribute to the pathogenesis of diseases such as cancers. In this review, we survey regulators of RTK signaling that tune receptor activity and intracellular transduction cascades, with a focus on the roles of these genes in the developing embryo. We detail the diverse inhibitory mechanisms utilized by negative feedback regulators that, when lost or perturbed, lead to aberrant increases in RTK signaling. We also discuss recent biochemical and genetic insights into positive regulators of RTK signaling and how these proteins function in tandem with negative regulators to guide embryonic development.

Indexed as

Embryonic DevelopmentGene Expression Regulation, DevelopmentalSignal TransductionAnimalsEmbryo, MammalianHumansNeoplasm ProteinsNeoplasmsReceptor Protein-Tyrosine KinasesNeoplasm ProteinsReceptor Protein-Tyrosine KinasesDevelopmental controlFeedback regulationRASopathiesReceptor tyrosine kinasesSignaling pathwaysSprouty

Identifiers

PMID29079424
PMCPMC5920792
OpenAlexW2765394809

What OpenQuestion holds

Textmetadata
LicenceTDM
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.