Evidence map›Paper›PMID 22397685›Full record

ArticleBMC physiology2012

Postnatal liver growth and regeneration are independent of c-myc in a mouse model of conditional hepatic c-myc deletion.

Jennifer A Sanders, Christoph Schorl, Ajay Patel, John M Sedivy, Philip A Gruppuso

Open access · hybridAbstract read
In one paragraph

Article in BMC physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

19 citing papers in PubMed, 38 citations in OpenAlex.

  1. Review
  2. Review
  3. Manipulating Myc for reparative regeneration.Frontiers in cell and developmental biology · 2024
    Review
  4. Review
  5. MYC-an emerging player in mitochondrial diseases.Frontiers in cell and developmental biology · 2023
    Review
  6. Lessons in aging from Myc knockout mouse models.Frontiers in cell and developmental biology · 2023
    Review
  7. Review
  8. Review
  9. Article
  10. Dual regulation ofThe Journal of cell biology · 2019
    Article
  11. Article
  12. Article
  13. Review
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. 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

5 authors at 2 institutions in 1 country.

Jennifer A SandersDepartment of Pediatrics, Rhode Island Hospital and Brown University, Providence, RI 02903, USA. Jennifer_Sanders@brown.edu
Christoph Schorl
Ajay Patel
John M Sedivy
Philip A Gruppuso
Brown University · USMacNeal Hospital · US

Funding

WNT SIGNALING IN HEPATOCELLULAR CARCINOMAP20RR015578 · NCRR · BROWN UNIVERSITY · PI THOMPSON, WILLIAM ALBERT · 2000 to 2009
$22.8M
UCP2 expression in colon cancerP20RR017695 · NCRR · RHODE ISLAND HOSPITAL (PROVIDENCE, RI) · PI RAMRATNAM, BHARAT · 2002 to 2011
$15.0M
REGULATION OF FETAL HEPATIC GROWTHR01HD024455 · NICHD · RHODE ISLAND HOSPITAL (PROVIDENCE, RI) · PI GRUPPUSO, PHILIP A. · 1989 to 2022
$7.9M
Effectors of cellular senescence statesR37AG016694 · NIA · BROWN UNIVERSITY · PI SEDIVY, JOHN M · 2009 to 2018
$3.2M
Nutritional Regulation of Fetal Liver DevelopmentR01HD035831 · NICHD · RHODE ISLAND HOSPITAL (PROVIDENCE, RI) · PI GRUPPUSO, PHILIP A. · 1999 to 2008
$1.6M
NCRR NIH HHS P20 RR015578NCRR NIH HHS P20 RR017695NCRR NIH HHS P20RR017695NIA NIH HHS R37 AG016694NICHD NIH HHS R01 HD024455NICHD NIH HHS R01HD24455NICHD NIH HHS R01HD35831PHS HHS R01FM041690
6 · The paper itself

Abstract

backgroundThe transcription factor c-myc regulates genes involved in hepatocyte growth, proliferation, metabolism, and differentiation. It has also been assigned roles in liver development and regeneration. In previous studies, we made the unexpected observation that c-Myc protein levels were similar in proliferating fetal liver and quiescent adult liver with c-Myc displaying nucleolar localization in the latter. In order to investigate the functional role of c-Myc in adult liver, we have developed a hepatocyte-specific c-myc knockout mouse, c-mycfl/fl;Alb-Cre.

resultsLiver weight to body weight ratios were similar in control and c-myc deficient mice. Liver architecture was unaffected. Conditional c-myc deletion did not result in compensatory induction of other myc family members or in c-Myc's binding partner Max. Floxed c-myc did have a negative effect on Alb-Cre expression at 4 weeks of age. To explore this relationship further, we used the Rosa26 reporter line to assay Cre activity in the c-myc floxed mice. No significant difference in Alb-Cre activity was found between control and c-mycfl/fl mice. c-myc deficient mice were studied in a nonproliferative model of liver growth, fasting for 48 hr followed by a 24 hr refeeding period. Fasting resulted in a decrease in liver mass and liver protein, both of which recovered upon 24 h of refeeding in the c-mycfl/fl;Alb-Cre animals. There was also no effect of reducing c-myc on recovery of liver mass following 2/3 partial hepatectomy.

conclusionsc-Myc appears to be dispensable for normal liver growth during the postnatal period, restoration of liver mass following partial hepatectomy and recovery from fasting.

Indexed as

AnimalsFemaleLiverMaleMiceMice, KnockoutRegenerationSalivary alpha-AmylasesAmy1 protein, mouseSalivary alpha-Amylases

Identifiers

PMID22397685
PMCPMC3353165
OpenAlexW2056165615

What OpenQuestion holds

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LicenceCC BY
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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.