Evidence map›Paper›PMID 24687993›Full record

ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2014

Fam65b is important for formation of the HDAC6-dysferlin protein complex during myogenic cell differentiation.

Anuradha Balasubramanian, Genri Kawahara, Vandana A Gupta, Anete Rozkalne, Ariane Beauvais, Louis M Kunkel, Emanuela Gussoni

Abstract read
In one paragraph

Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2014. 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
1.3field-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

25 citing papers in PubMed, 31 citations in OpenAlex.

  1. Article
  2. Article
  3. A Novel Dysferlin-Binding Kinase CK2α Promotes Plasma Membrane Repair in Dysferlinopathy.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  4. Cold-Induced Suppression of Myogenesis in Skeletal Muscle Stem Cells Contributes to Delayed Muscle Regeneration During Hibernation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    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

7 authors at 3 institutions in 2 countries.

Anuradha BalasubramanianProgram in Genomics, Division of Genetics and.
Genri KawaharaProgram in Genomics, Division of Genetics and.
Vandana A GuptaProgram in Genomics, Division of Genetics and.
Anete RozkalneProgram in Genomics, Division of Genetics and.
Ariane BeauvaisRegenerative Medicine Program, Ottawa Hospital Research Institute, Ottawa, Ontario, Canada; and.
Louis M KunkelProgram in Genomics, Division of Genetics and Manton Center for Orphan Disease Research, Boston Children's Hospital, Boston, Massachusetts, USA; Harvard Medical School, Boston, Massachusetts, USA.
Emanuela GussoniProgram in Genomics, Division of Genetics and Harvard Medical School, Boston, Massachusetts, USA gussoni@enders.tch.harvard.edu.
Boston Children's Hospital · USBoston Children's Museum · USOttawa Hospital · CA

Funding

C6ORF32, AN HDAC6-BINDING PROTEIN THAT REGULATES MYOBLAST DIFFERENTIATIONR01AR060317 · NIAMS · BOSTON CHILDREN'S HOSPITAL · PI GUSSONI, EMANUELA · 2011 to 2015
$1.9M
Roles of RNA helicase and ribosomal biogenesis in normal and diseased muscleK01AR062601 · NIAMS · BRIGHAM AND WOMEN'S HOSPITAL · PI GUPTA, VANDANA · 2012 to 2016
$647k
NIAMS NIH HHS 1R01AR060317-01NIAMS NIH HHS K01 AR062601NIAMS NIH HHS R01 AR060317
6 · The paper itself

Abstract

Previously, we identified family with sequence similarity 65, member B (Fam65b), as a protein transiently up-regulated during differentiation and fusion of human myogenic cells. Silencing of Fam65b expression results in severe reduction of myogenin expression and consequent lack of myoblast fusion. The molecular function of Fam65b and whether misregulation of its expression could be causative of muscle diseases are unknown. Protein pulldowns were used to identify Fam65b-interacting proteins in differentiating human muscle cells and regenerating muscle tissue. In vitro, human muscle cells were treated with histone-deacetylase (HDAC) inhibitors, and expression of Fam65b and interacting proteins was studied. Nontreated cells were used as controls. In vivo, expression of Fam65b was down-regulated in developing zebrafish to determine the effects on muscle development. Fam65b binds to HDAC6 and dysferlin, the protein mutated in limb girdle muscular dystrophy 2B. The tricomplex Fam65b-HDAC6-dysferlin is transient, and Fam65b expression is necessary for the complex to form. Treatment of myogenic cells with pan-HDAC or HDAC6-specific inhibitors alters Fam65b expression, while dysferlin expression does not change. Inhibition of Fam65b expression in developing zebrafish results in abnormal muscle, with low birefringence, tears at the myosepta, and increased embryo lethality. Fam65b is an essential component of the HDAC6-dysferlin complex. Down-regulation of Fam65b in developing muscle causes changes consistent with muscle disease.-Balasubramanian, A., Kawahara, G., Gupta, V. A., Rozkalne, A., Beauvais, A., Kunkel, L. M., Gussoni, E. Fam65b is important for formation of the HDAC6-dysferlin protein complex during myogenic cell differentiation.

Indexed as

Amino Acid SequenceAnimalsCell Adhesion MoleculesCell DifferentiationCells, CulturedDown-RegulationDysferlinHistone Deacetylase 6Histone DeacetylasesHumansMembrane ProteinsMiceMice, Inbred C57BLMolecular Sequence DataMuscle CellsMuscle DevelopmentCell Adhesion MoleculesDysferlinDYSF protein, humanHDAC6 protein, humanHistone Deacetylase 6Histone DeacetylasesMembrane ProteinsMuscle ProteinsProteinsRIPOR2 protein, humanTubulinacetylationmuscular dystrophymyoblastzebrafish

Identifiers

PMID24687993
PMCPMC4062822
OpenAlexW2136750459

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.