Ask about this productRelated genes to: PAX7 antibody
- Gene:
- PAX7 NIH gene
- Name:
- paired box 7
- Previous symbol:
- -
- Synonyms:
- Hup1
- Chromosome:
- 1p36.13
- Locus Type:
- gene with protein product
- Date approved:
- 1992-11-20
- Date modifiied:
- 2014-11-18
Related products to: PAX7 antibody
Related articles to: PAX7 antibody
- Melatonin (N‑acetyl‑5‑methoxytryptamine), traditionally viewed as a pineal neurohormone regulating circadian rhythms, is now recognized as a pleiotropic molecule with significant implications for musculoskeletal (MSK) health. Its receptor‑dependent and receptor‑independent actions influence bone, cartilage, muscle, tendon, ligament, and spine biology, positioning melatonin as a potential therapeutic agent across diverse MSK pathologies. - Source: PubMed
Publication date: 2026/05/11
Jeyaraman MadhanJeyaraman NaveenSridhar Aadithya SiddarthRamasubramanian SwaminathanNallakumarasamy ArulkumarMuthu Sathish - Muscle stem cells orchestrate skeletal muscle regeneration through complex fate decisions. The transcriptional co-activators Yes-associated protein 1 (YAP) and WW domain-containing transcription regulator 1 (TAZ) contribute to multiple stages of myogenesis, yet their individual contributions to regeneration remain unclear due to substantial functional overlap. We genetically titrated YAP and TAZ expression in MuSCs with double knockout and single allele mutants by crossing Pax7 mice with TAZ ;YAP mice. Conditional deletion of both YAP and TAZ in muscle stem cells severely disrupted muscle regeneration with dramatically increased fibrosis and impaired myofiber formation following injury. In contrast, a single allele of either YAP or TAZ was sufficient to rescue injured muscle weight and myofiber cross-sectional area. Similarly, the reduced proliferation of double knockout muscle stem cells on isolated myofibers was restored by a single allele of either YAP or TAZ. In addition, disrupted actin cytoskeleton organization and reduced focal adhesion formation drove double knockout muscle stem cell migration defects, negatively impacting muscle stem cell congregation prior to fusion. Thus, YAP and TAZ function redundantly as critical transcriptional co-activators to regulate progenitor proliferation and migration during muscle regeneration. By challenging myogenesis with double knockout of both YAP and TAZ, we unmasked regenerative requirements previously undetected in single-gene loss models, highlighting genetic redundancy as a key principle buffering regenerative robustness. - Source: PubMed
Publication date: 2026/09/07
Silver Jason SCutler Alicia AChang Tze-LingAnseth Kristi SOlwin Bradley B - Volumetric muscle loss (VML) represents a significant unmet clinical need in current medical practice. Decellularized extracellular matrix (dECM) offers a promising clinical approach. However, its inherent architecture impedes adaptive topological guidance for rapid cellular infiltration, spatial organization, and coordinated immune response, limiting functional restoration. Here, we report a dECM yarn scaffold (YS) fabricated by 3D weaving of rotary-cut yarns, achieving precise structural control, full interconnectivity and high porosity. In murine VML models, YS significantly improved vascularization, innervation, muscle mass, and strength restoration. Single-nucleus RNA-sequencing identified decreased SPP1 neutrophil infiltration alongside increased CD206/IGF-1 macrophages, whose enhanced IGF-1 secretion stimulated PAX7 muscle cell growth via amplified IGF-1R signaling. The robust regenerative efficacy and translational potential of YS was further confirmed in a canine VML model. Our study shows that restructured dECM scaffolds address structural constraints to enable effective in situ muscle regeneration, while simultaneously establishing a novel scaffold platform for regenerative medicine. - Source: PubMed
Publication date: 2026/08/29
Song GuangzhouCong WenqianLu HongjiangWang YumengZhao YanzhenWang ShaowenZhu ShijieFan MengKong DelingWang KaiZhou XinZhu Meifeng - Skeletal muscles contain myogenic and non-myogenic progenitor cells that proliferate and differentiate after tissue damage to restore myofiber, connective tissue, and blood vessel homeostasis. We previously showed that cancer-induced muscle wasting involves myofiber damage and impaired differentiation of myogenic progenitors, coincident with the aberrant accumulation of mesenchymal progenitor cells expressing both myogenic (Pax7) and non-myogenic (Sca1, Pdgfrα) progenitor markers. Here, we combined lineage tracing and scRNA-seq to more deeply explore muscle resident progenitor cells during cancer cachexia. Colon-26 (C-26) carcinoma cells were injected into adult (≥12-weeks-old) Pax7-Cre; Rosa26-LSL-tdTomato mice, and tamoxifen was administered after tumors were established but prior to cachexia. At cachexia endpoint, scRNA-seq analysis was performed on muscle mononuclear cells. In both control and C-26 muscles, and transcripts were restricted to myogenic progenitors, whereas and were restricted to non-myogenic progenitors. These results were confirmed by flow cytometry and suggest that mesenchymal progenitor cells do not commit to a myogenic fate during cancer cachexia. However, consistent with earlier findings, our transcriptomic analyses validated that myogenic progenitors from tumor-bearing mice were impaired to differentiate. When we repeated Pax7-lineage tracing and scRNA-seq on young mice (6-week-old) still undergoing developmental muscle growth similar results were obtained, but interestingly, by flow cytometry we detected a small population of Sca1; tdTomato cells, not present in adult muscles. Thus, non-myogenic progenitors might indeed be capable of adopting a myogenic fate during cancer cachexia, but this contributes to only a minor fraction of Pax7 cells and likely to be age dependent. - Source: PubMed
Publication date: 2026/09/19
Miller Spencer GUdeme Abasi-AmaFunk EmmaAlfaro-Quinde CarlosSubramanian SuganyaBerto StefanoOuyang JianWang David JOstrowski Michael CZimmers Teresa AGuttridge Denis C - Skeletal muscle fibers are largely post-mitotic in adulthood yet retain robust regenerative capacity through satellite cells (SCs), quiescent muscle stem cells located beneath the basal lamina that are activated after injury, proliferate as myoblasts, differentiate, fuse into myotubes, and mature via tightly regulated cues. Given the burden of muscle-wasting and neuromuscular diseases, including Duchenne muscular dystrophy (DMD) (driven by dystrophin defects and impaired SC function), amyotrophic lateral sclerosis (ALS) (with progressive atrophy and evidence of SC perturbation), and myasthenia gravis (autoimmune neuromuscular junction failure), physiologically relevant and scalable in vitro SC systems are essential for mechanistic studies and future cell-therapy development. This review revisits culture conditions and workflows used to isolate, enrich, and differentiate rodent and human skeletal muscle progenitors, integrating key regenerative signalling (hepatocyte growth factor (HGF)/mesenchymal-epithelial transition factor (c-Met), nitric oxide (NO), fibroblast growth factor (FGF)-mitogen-activated protein kinase (MAPK) modulated by Sprouty-1, insulin-like growth factor (IGF)-driven Akt/mechanistic target of rapamycin (mTOR) hypertrophy, inflammatory cytokines including interleukin-6 (IL-6) signal transducer and activator of transcription 3 (STAT3)-cyclin D1, and differentiation switches involving Notch/Wnt, glycogen synthase kinase 3 (GSK3), and mitogen-activated protein kinase (p38α MAPK)) with practical culture variables. Two principal isolation strategies are compared: explant outgrowth, which preserves tissue architecture and injury-mimicking activation but can be slow and yield-limited without matrix support, and enzymatic dissociation (e.g., collagenase, dispase, pronase, protease XIV), which accelerates release from the basal lamina and supports high-throughput needs but requires optimization to minimize trauma and fibroblast contamination. Across reported protocols, matrix choice (notably Matrigel or poly-L-lysine/Matrigel), differential pre-plating, and medium composition (serum levels, chick embryo extract (CEE), basic fibroblast growth factor (bFGF)) strongly influence SC quiescence, migration, survival, and myotube formation, with high purities achievable (e.g., ~97.6% Pax7 after explant plus differential adherence; ~90% α7-integrin positive while lacking SCA-1, CD31, and CD45; up to ~98% after preplating; and ~95% in several optimized workflows) and differentiation occurring within ~1-7 days depending on conditions. The isolation of human SCs is constrained by the limited availability of tissue, inconsistent biopsy quality, and the absence of reliable markers to differentiate SCs from other mononuclear cells. Induced pluripotent stem cell (iPSC)-derived muscle organoids present a patient-specific alternative; however, they predominantly produce fetal-like instead of mature adult SCs. Overall, explant-based systems best retain physiological fidelity for niche and matrix studies, whereas enzymatic and hybrid approaches maximize efficiency and yield, underscoring that culture strategy should be selected based on the experimental objective rather than presumed universal superiority. - Source: PubMed
Publication date: 2026/09/23
Kumari PoojaRaval AayushiRana PranavKaushik Rishabh RaiSahi Ajay KumarGundu ShravanyaMahto Sanjeev Kumar