ArticleMolecular cell2007
Functional interdependence at the chromatin level between the MKK6/p38 and IGF1/PI3K/AKT pathways during muscle differentiation.
Article in Molecular cell, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 116 papers.
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.
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.
Who cites it
116 citing papers in PubMed, 193 citations in OpenAlex.
- Chromatin modifiers KMT2D, cBAF, and p300 cooperatively facilitate de novo binding of transcription factors on enhancers.Nature communications · 2026Article
- The Evolutionarily Conserved TPM1 Super-Enhancer Drives Skeletal Muscle Regeneration via Mechanotransduction Signaling.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- MRG15 decline in aged/injured MuSCs hinders regeneration via differentiation defects.Cell regeneration (London, England) · 2026Article
- MYOD represses gene expression from non-E-box motifs.Genes & development · 2025Article
- Cancer-Associated Fibroblasts Foster a High-Lactate Microenvironment to Drive Perineural Invasion in Pancreatic Cancer.Cancer research · 2025Article
- E-box independent chromatin recruitment turns MYOD into a transcriptional repressor.bioRxiv : the preprint server for biology · 2024Article
- Promoting and accelerating muscle regeneration through cell therapy in a mouse model.Journal of Taibah University Medical Sciences · 2024Article
- Unlocking the potential of exercise: harnessing myokines to delay musculoskeletal aging and improve cognitive health.Frontiers in physiology · 2024Review
- Effect of Zinc Amino Acid Complexes on Growth Performance, Tissue Zinc Concentration, and Muscle Development of Broilers.Biological trace element research · 2024Article
- Ginsenoside Rg5 promotes muscle regeneration via p38MAPK and Akt/mTOR signaling.Journal of ginseng research · 2023Article
- DNA-PKcs regulates myogenesis in an Akt-dependent manner independent of induced DNA damage.Cell death and differentiation · 2023Article
- Decrotonylation of AKT1 promotes AKT1 phosphorylation and activation during myogenic differentiation.Journal of advanced research · 2023Article
- Article
- Regulation of the Wnt signaling pathway during myogenesis by the mammalian SWI/SNF ATPase BRG1.Frontiers in cell and developmental biology · 2023Article
- Review
- Anti‑oncogenic and pro‑myogenic action of the MKK6/p38/AKT axis induced by targeting MEK/ERK in embryonal rhabdomyosarcoma.Oncology reports · 2022Article
- Review
- Review
- CCL7 and TGF-β secreted by MSCs play opposite roles in regulating CRC metastasis in a KLF5/CXCL5-dependent manner.Molecular therapy : the journal of the American Society of Gene Therapy · 2022Article
- VEGFB Promotes Myoblasts Proliferation and Differentiation through VEGFR1-PI3K/Akt Signaling Pathway.International journal of molecular sciences · 2021Article
56 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 5 institutions in 2 countries.
Funding
Abstract
During muscle regeneration, the mechanism integrating environmental cues at the chromatin of muscle progenitors is unknown. We show that inflammation-activated MKK6-p38 and insulin growth factor 1 (IGF1)-induced PI3K/AKT pathways converge on the chromatin of muscle genes to target distinct components of the muscle transcriptosome. p38 alpha/beta kinases recruit the SWI/SNF chromatin-remodeling complex; AKT1 and 2 promote the association of MyoD with p300 and PCAF acetyltransferases, via direct phosphorylation of p300. Pharmacological or genetic interference with either pathway led to partial assembly of discrete chromatin-bound complexes, which reflected two reversible and distinct cellular phenotypes. Remarkably, PI3K/AKT blockade was permissive for chromatin recruitment of MEF2-SWI/SNF complex, whose remodeling activity was compromised in the absence of MyoD and acetyltransferases. The functional interdependence between p38 and IGF1/PI3K/AKT pathways was further established by the evidence that blockade of AKT chromatin targets was sufficient to prevent the activation of the myogenic program triggered by deliberate activation of p38 signaling.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.