Evidence map›Paper›PMID 19447101›Full record

ArticleDevelopmental biology2009

Kit signaling via PI3K promotes ovarian follicle maturation but is dispensable for primordial follicle activation.

George B John, Meredith J Shidler, Peter Besmer, Diego H Castrillon

Open access · greenAbstract read
In one paragraph

Article in Developmental biology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed, 1 pooled it
7.5field-weighted citation impact, top 3% 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

51 citing papers in PubMed, 1 synthesis or guideline pooled it, 118 citations in OpenAlex.

  1. Biomechanics and mechanical signaling in the ovary: a systematic review.Journal of assisted reproduction and genetics · 2018
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  14. Mechanism of Zuogui pill enhancing ovarian function and skin elastic repair in premature aging rats based on artificial intelligence medical image analysis.Skin research and technology : official journal of International Society for Bioengineering and the Skin (ISBS) [and] International Society for Digital Imaging of Skin (ISDIS) [and] International Society for Skin Imaging (ISSI) · 2024
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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 2 institutions in 1 country.

George B JohnDepartment of Pathology and Simmons Comprehensive Cancer Center, University of Texas Southwestern Medical Center, Dallas, 75390-9072, USA.
Meredith J Shidler
Peter Besmer
Diego H Castrillon
The University of Texas Southwestern Medical Center · USMemorial Sloan Kettering Cancer Center · US

Funding

Regulation of Ovarian Follicle ActivationR01HD048690 · NICHD · UT SOUTHWESTERN MEDICAL CENTER · PI CASTRILLON, DIEGO H · 2005 to 2009
$1.7M
Mentoring and Research in Mouse Models of Cancer and InfertilityK26RR024196 · NCRR · UT SOUTHWESTERN MEDICAL CENTER · PI CASTRILLON, DIEGO H · 2007 to 2011
$616k
NCRR NIH HHS K26 RR024196NCRR NIH HHS K26RR024196NICHD NIH HHS R01 HD048690NICHD NIH HHS R01HD048690
6 · The paper itself

Abstract

In mammals, primordial follicles are generated early in life and remain dormant for prolonged intervals. Their growth resumes via a process known as primordial follicle activation. Recent genetic studies have demonstrated that phosphoinositide 3-kinase (PI3K) is the essential signaling pathway controlling this process throughout life, acting via Akt to regulate nucleocytoplasmic shuttling of Foxo3, which functions as a downstream molecular switch. The receptor tyrosine kinase Kit has been implicated by numerous studies as the critical upstream regulator of primordial follicle activation via PI3K/Akt. Here we present a genetic analysis of the contribution of Kit in regulating primordial follicle activation and early follicle growth, employing a knock-in mutation (Kit(Y719F)) that completely abrogates signaling via PI3K. Surprisingly, homozygous Kit(Y719F) female mice undergo primordial follicle activation and are fertile, demonstrating that Kit signaling via PI3K is dispensable for this process. However, other abnormalities were identified in Kit(Y719F) ovaries, including accelerated primordial follicle depletion and accumulation of morphologically abnormal primary/secondary follicles with persistent nuclear Foxo3 localization. These findings reveal specific roles of Kit in the maintenance of the primordial follicle reserve and in the primary to secondary follicle transition, but argue that Kit is dispensable in primordial follicle activation.

Indexed as

AnimalsAnimals, NewbornFemaleGene Knock-In TechniquesMiceMutationOvarian FollicleOvaryPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-kitSignal TransductionPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-kit

Identifiers

PMID19447101
PMCPMC2726617
OpenAlexW2059844002

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.