Evidence map›Paper›PMID 26296887›Full record

ArticleThe Journal of biological chemistry2015

Lipin1 Regulates Skeletal Muscle Differentiation through Extracellular Signal-regulated Kinase (ERK) Activation and Cyclin D Complex-regulated Cell Cycle Withdrawal.

Weihua Jiang, Jing Zhu, Xun Zhuang, Xiping Zhang, Tao Luo, Karyn A Esser, Hongmei Ren

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.5field-weighted citation impact, top 17% 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

25 citing papers in PubMed, 35 citations in OpenAlex.

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  10. Molecular genetics and metabolism reports · 2022
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  14. Review
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  17. Review
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  19. Article
  20. Loss of lipin 1-mediated phosphatidic acid phosphohydrolase activity in muscle leads to skeletal myopathy in mice.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019
    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 at 1 institution in 1 country.

Weihua JiangFrom the Division of Cardiovascular Medicine, Department of Internal Medicine, Saha Cardiovascular Center.
Jing ZhuFrom the Division of Cardiovascular Medicine, Department of Internal Medicine, Saha Cardiovascular Center.
Xun ZhuangFrom the Division of Cardiovascular Medicine, Department of Internal Medicine, Saha Cardiovascular Center.
Xiping ZhangDepartment of Physiology, University of Kentucky, Lexington, Kentucky 40536.
Tao LuoFrom the Division of Cardiovascular Medicine, Department of Internal Medicine, Saha Cardiovascular Center.
Karyn A EsserDepartment of Physiology, University of Kentucky, Lexington, Kentucky 40536.
Hongmei RenFrom the Division of Cardiovascular Medicine, Department of Internal Medicine, Saha Cardiovascular Center, hongmei.ren@uky.edu.
University of Kentucky · US

Funding

The role of IKKß in linking obesity to adipose tissue inflammation and adipogeneP20GM103527 · NIGMS · UNIVERSITY OF KENTUCKY · PI MORRIS, ANDREW J · 2012 to 2017
$13.7M
BetaCatenin Regulation of Skeletal Muscle HypertrophyR01AR061939 · NIAMS · UNIVERSITY OF KENTUCKY · PI ESSER, KARYN A, MCCARTHY, JOHN JOSEPH · 2012 to 2016
$1.7M
NIAMS NIH HHS AR061939NIAMS NIH HHS R01 AR061939NIGMS NIH HHS P20 GM103527NIGMS NIH HHS P20 GM103527-06
6 · The paper itself

Abstract

Lipin1, an intracellular protein, plays critical roles in controlling lipid synthesis and energy metabolism through its enzymatic activity and nuclear transcriptional functions. Several mouse models of skeletal muscle wasting are associated with lipin1 mutation or altered expression. Recent human studies have suggested that children with homozygous null mutations in the LPIN1 gene suffer from rhabdomyolysis. However, the underlying pathophysiologic mechanism is still poorly understood. In the present study we examined whether lipin1 contributes to regulating muscle regeneration. We characterized the time course of skeletal muscle regeneration in lipin1-deficient fld mice after injury. We found that fld mice exhibited smaller regenerated muscle fiber cross-sectional areas compared with wild-type mice in response to injury. Our results from a series of in vitro experiments suggest that lipin1 is up-regulated and translocated to the nucleus during myoblast differentiation and plays a key role in myogenesis by regulating the cytosolic activation of ERK1/2 to form a complex and a downstream effector cyclin D3-mediated cell cycle withdrawal. Overall, our study reveals a previously unknown role of lipin1 in skeletal muscle regeneration and expands our understanding of the cellular and molecular mechanisms underlying skeletal muscle regeneration.

Indexed as

Cell CycleAnimalsCell DifferentiationCyclin DCyclin-Dependent Kinase 6Extracellular Signal-Regulated MAP KinasesMiceMuscle, SkeletalMyoblastsNuclear ProteinsOrgan SizePhosphatidate PhosphatasePhosphorylationCdk6 protein, mouseCyclin DCyclin-Dependent Kinase 6Extracellular Signal-Regulated MAP KinasesLpin1 protein, mouseNuclear ProteinsPhosphatidate Phosphatasecell cycleERKlipin1muscle regenerationmyoblast differentiationnuclear translocationprotein phosphorylationskeletal muscle

Identifiers

PMID26296887
PMCPMC4583021
OpenAlexW2289141937

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.