Evidence map›Paper›PMID 26957088›Full record

ReviewHistology and histopathology2016

Mammalian target of rapamycin complex (mTOR) pathway modulates blood-testis barrier (BTB) function through F-actin organization and gap junction.

Nan Li, C Yan Cheng

Abstract readReview
In one paragraph

Review in Histology and histopathology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.4field-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

23 citing papers in PubMed, 41 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Inhibition of LncRNAInternational journal of molecular sciences · 2025
    Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. Mechanisms of Male Reproductive Toxicity of Polybrominated Diphenyl Ethers.International journal of molecular sciences · 2022
    Review
  10. Rapamycin Ameliorates Radiation-Induced Testis Damage in Mice.Frontiers in cell and developmental biology · 2022
    Article
  11. Review
  12. Article
  13. Review
  14. Review
  15. UropathogenicFrontiers in immunology · 2021
    Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review
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

2 authors at 1 institution in 1 country.

Nan LiThe Mary M. Wohlford Laboratory for Male Contraceptive Research, Center for Biomedical Research, Population Council, New York, New York, USA.
C Yan ChengThe Mary M. Wohlford Laboratory for Male Contraceptive Research, Center for Biomedical Research, Population Council, New York, New York, USA. ccheng@rockefeller.edu or y-cheng@popcbr.rockefeller.edu.
Population Council · US

Funding

SPECIALIZED CONTRACEPTIVE DEVELOPMENT RESEARCH CENTERU54HD029990 · NICHD · POPULATION COUNCIL · PI MORRIS, PATRICIA L · 1992 to 2016
$27.7M
The biology of blood-testis barrier dynamicsR01HD056034 · NICHD · POPULATION COUNCIL · PI CHENG, C. YAN · 2009 to 2018
$3.4M
Junction Dynamics and Male Fertility RegulationU01HD045908 · NICHD · POPULATION COUNCIL · PI CHENG, C. YAN · 2004 to 2008
$1.3M
NICHD NIH HHS R01 HD056034NICHD NIH HHS U01 HD045908NICHD NIH HHS U54 HD029990
6 · The paper itself

Abstract

mTOR (mammalian target of rapamycin) is one of the most important signaling molecules in mammalian cells which regulates an array of cellular events, ranging from cell metabolism to cell proliferation. Based on the association of mTOR with the core component proteins, such as Raptor or Rictor, mTOR can become the mTORC1 (mammalian target of rapamycin complex 1) or mTORC2, respectively. Studies have shown that during the epithelial cycle of spermatogenesis, mTORC1 promotes remodeling and restructuring of the blood-testis barrier (BTB) in vitro and in vivo, making the Sertoli cell tight junction (TJ)-permeability barrier "leaky"; whereas mTORC2 promotes BTB integrity, making the Sertoli cell TJ-barrier "tighter". These contrasting effects, coupled with the spatiotemporal expression of the core signaling proteins at the BTB that confer the respective functions of mTORC1 vs. mTORC2 thus provide a unique mechanism to modulate BTB dynamics, allowing or disallowing the transport of biomolecules and also preleptotene spermatocytes across the immunological barrier. More importantly, studies have shown that these changes to BTB dynamics conferred by mTORC1 and mTORC2 are mediated by changes in the organization of the actin microfilament networks at the BTB, and involve gap junction (GJ) intercellular communication. Since GJ has recently been shown to be crucial to reboot spermatogenesis and meiosis following toxicant-induced aspermatogenesis, these findings thus provide new insightful information regarding the integration of mTOR and GJ to regulate spermatogenesis.

Indexed as

ActinsAnimalsBlood-Testis BarrierGap JunctionsHumansMaleSignal TransductionSpermatogenesisTOR Serine-Threonine KinasesActinsTOR Serine-Threonine Kinases

Identifiers

PMID26957088
PMCPMC4938759
OpenAlexW2417027827

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.