Evidence map›Paper›PMID 27206316›Full record

ArticleCell death and differentiation2016

Focused screening of mitochondrial metabolism reveals a crucial role for a tumor suppressor Hbp1 in ovarian reserve.

Z Dong, M Huang, Z Liu, P Xie, Y Dong, X Wu, Z Qu, B Shen, X Huang, T Zhang and 5 more

Open access · hybridAbstract read
In one paragraph

Article in Cell death and differentiation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

22 citing papers in PubMed, 37 citations in OpenAlex.

  1. Review
  2. Mitochondrial function meets oncology: the multifaceted role of TFAM across cancer types.Apoptosis : an international journal on programmed cell death · 2026
    Review
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  4. Review
  5. Review
  6. The epithelial NaCell communication and signaling : CCS · 2024
    Article
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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

15 authors at 4 institutions in 3 countries.

Z DongMOE Key Laboratory of Model Animal for Disease Study, Model Animal Research Center, Nanjing University, Nanjing, China.
M HuangCambridge-Suda Genomic Research Center, Soochow University, Suzhou, China.
Z LiuCambridge-Suda Genomic Research Center, Soochow University, Suzhou, China.
P XieMOE Key Laboratory of Model Animal for Disease Study, Model Animal Research Center, Nanjing University, Nanjing, China.
Y DongCambridge-Suda Genomic Research Center, Soochow University, Suzhou, China.
X WuMOE Key Laboratory of Model Animal for Disease Study, Model Animal Research Center, Nanjing University, Nanjing, China.
Z QuMOE Key Laboratory of Model Animal for Disease Study, Model Animal Research Center, Nanjing University, Nanjing, China.
B ShenMOE Key Laboratory of Model Animal for Disease Study, Model Animal Research Center, Nanjing University, Nanjing, China.
X HuangMOE Key Laboratory of Model Animal for Disease Study, Model Animal Research Center, Nanjing University, Nanjing, China.
T ZhangCambridge-Suda Genomic Research Center, Soochow University, Suzhou, China.
J LiState Key Laboratory of Reproductive Medicine, Nanjing Medical University, Nanjing, China.
J LiuMOE Key Laboratory of Model Animal for Disease Study, Model Animal Research Center, Nanjing University, Nanjing, China.
T YanaseDepartment of Endocrinology and Diabetes Mellitus, School of Medicine, Fukuoka University, Fukuoka, Japan.
C ZhouDepartment of Biochemistry and Molecular Medicine and Comprehensive Cancer Center, Institute for Pediatric Regenerative Medicine, University of California Davis, School of Medicine, Sacramento, CA, USA.
Y XuMOE Key Laboratory of Model Animal for Disease Study, Model Animal Research Center, Nanjing University, Nanjing, China.ORCID 0000-0002-6689-7768
Model Animal Research Center · CNSoochow University · CNCalifornia Institute for Regenerative Medicine · USFukuoka University · JP

Funding

Wnt Signaling in Craniofacial Developmental DisordersR01DE021696 · NIDCR · UNIVERSITY OF CALIFORNIA AT DAVIS · PI ZHOU, CHENGJI · 2011 to 2015
$1.9M
NIDCR NIH HHS R01 DE021696
6 · The paper itself

Abstract

Granulosa cells (GCs) are tightly associated with fertility and the fate of ovarian follicles. Mitochondria are the central executers of apoptosis. However, the genetic basis underlying mitochondrial modulation in GCs during the ovarian development is poorly understood. Here, CRISPR/Cas9-mediated genetic screening was used to identify genes conferring mitochondrial metabolism in human GCs. The results uncovered roles for several tumor suppressors, including HBP1, in the augmentation of mitochondrial function. Focused analysis revealed that high-mobility group (HMG)-box transcription factor 1 (Hbp1) levels regulate mitochondrial biogenesis, which is associated with global changes in transcription including Tfam. The systemic or granulosa-specific but not oocyte-specific ablation of Hbp1 promoted follicle growth and oocyte production, and is associated with the reduced apoptotic signals in mouse GCs. Consistent with increased mitochondrial function and attenuated GC apoptosis, the regulation of Hbp1 conferred substantial protection of ovarian reserve. Thus, the results of the present study provide a critical target to understand the control of the reproductive lifespan.

Indexed as

Ovarian ReserveAgingAnimalsApoptosisCell LineCell RespirationCRISPR-Cas SystemsEnergy MetabolismFemaleFertilityFollicular AtresiaGene DeletionGene Expression RegulationGene Knockout TechniquesGenes, Tumor SuppressorGranulosa CellsHbp1 protein, mouseHigh Mobility Group ProteinsRepressor ProteinsTumor Suppressor Proteins

Identifiers

PMID27206316
PMCPMC5041189
OpenAlexW2396321838

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.