Evidence map›Paper›PMID 26703468›Full record

ArticleThe Journal of biological chemistry2016

SOCS2 Balances Metabolic and Restorative Requirements during Liver Regeneration.

Ryota Masuzaki, Sophia Zhao, M Todd Valerius, Daisuke Tsugawa, Yuki Oya, Kevin C Ray, Seth J Karp

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in The Journal of biological chemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
–field-weighted citation impact
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

14 citing papers in PubMed.

  1. Review
  2. Insights into the mechanisms of angiogenesis in hepatoblastoma.Frontiers in cell and developmental biology · 2025
    Review
  3. Article
  4. Article
  5. Review
  6. Semi-Lethal Primary Ciliary Dyskinesia in Rats Lacking theInternational journal of molecular sciences · 2021
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. The suppressor of cytokine signaling 2 (SOCS2) inhibits tumor metastasis in hepatocellular carcinoma.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Article
  14. 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.

Ryota MasuzakiFrom the Transplant Center, Department of Surgery, Vanderbilt University Medical Center, Nashville, Tennessee 37232.
Sophia ZhaoDepartment of Genetics, Harvard Medical School, Boston, Massachusetts 02115.
M Todd ValeriusRenal Division, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115, and Harvard Stem Cell Institute, Harvard University, Cambridge, Massachusetts 02138.
Daisuke TsugawaFrom the Transplant Center, Department of Surgery, Vanderbilt University Medical Center, Nashville, Tennessee 37232.
Yuki OyaFrom the Transplant Center, Department of Surgery, Vanderbilt University Medical Center, Nashville, Tennessee 37232.
Kevin C RayFrom the Transplant Center, Department of Surgery, Vanderbilt University Medical Center, Nashville, Tennessee 37232.
Seth J KarpFrom the Transplant Center, Department of Surgery, Vanderbilt University Medical Center, Nashville, Tennessee 37232, seth.karp@vanderbilt.edu.

Funding

Translational Analysis CoreP30DK058404 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI RICHARD M. PEEK · 2002 to 2026
$29.9M
BMP Signaling--A Therapeutic Target in Liver DiseaseR01DK081387 · NIDDK · VANDERBILT UNIVERSITY · PI KARP, SETH J · 2010 to 2014
$1.7M
NIDDK NIH HHS 7R01DK081387NIDDK NIH HHS P30 DK058404NIDDK NIH HHS R01 DK081387
6 · The paper itself

Abstract

After significant injury, the liver must maintain homeostasis during the regenerative process. We hypothesized the existence of mechanisms to limit hepatocyte proliferation after injury to maintain metabolic and synthetic function. A screen for candidates revealed suppressor of cytokine signaling 2 (SOCS2), an inhibitor of growth hormone (GH) signaling, was strongly induced after partial hepatectomy. Using genetic deletion and administration of various factors we investigated the role of SOCS2 during liver regeneration. SOCS2 preserves liver function by restraining the first round of hepatocyte proliferation after partial hepatectomy by preventing increases in growth hormone receptor (GHR) via ubiquitination, suppressing GH pathway activity. At later times, SOCS2 enhances hepatocyte proliferation by modulating a decrease in serum insulin-like growth factor 1 (IGF-1) that allows GH release from the pituitary. SOCS2, therefore, plays a dual role in modulating the rate of hepatocyte proliferation. In particular, this is the first demonstration of an endogenous mechanism to limit hepatocyte proliferation after injury.

Indexed as

Liver RegenerationUbiquitinationAnimalsCell ProliferationCells, CulturedGene Expression RegulationGrowth HormoneHepatectomyImmunohistochemistryInsulin-Like Growth Factor ILiverMaleMice, Inbred C57BLMice, KnockoutPituitary GlandProtein TransportGrowth Hormoneinsulin-like growth factor-1, mouseInsulin-Like Growth Factor IReceptors, SomatotropinSocs2 protein, mouseSuppressor of Cytokine Signaling Proteinsgrowth hormoneinsulin-like growth factor (IGF)liver injuryregenerationsocs2ubiquitylation (ubiquitination)

Identifiers

PMID26703468
PMCPMC4751379

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.