| 2004 |
Mustang (MUSTN1) encodes an 82 amino acid nuclear protein with no homology to any known protein family. Nuclear localization was confirmed experimentally using a GFP-Mustang fusion protein expressed in cells. |
GFP fusion protein expression and fluorescence microscopy; in situ hybridization; cloning and expression assays |
FASEB journal |
Medium |
14718386
|
| 2006 |
The Mustang promoter contains functional AP-1 and AP-2 binding sites; one specific AP-1 site is required for substantial transcriptional activation (its deletion or mutation decreases activity by 32–40%). In proliferating and differentiating C2C12 myoblasts, c-Fos, Fra-2, and JunD are the AP-1 factors that bind this site and drive transcriptional activation. |
Promoter deletion and mutation constructs; luciferase reporter assays; EMSA (electrophoretic mobility shift assay) in C2C12 cells |
Bone |
High |
16731063
|
| 2009 |
Mustn1 is necessary for chondrocyte proliferation and differentiation in vitro. Silencing Mustn1 in RCJ3.1C5.18 pre-chondrocytic cells significantly reduced proliferation (~55–75% reduction) and proteoglycan matrix production (~34–40% less), with concomitant downregulation of chondrogenic markers Sox9, Collagen type II, and Collagen type X. Reintroduction of Mustn1 into silenced cells rescued proliferation rate, matrix production, and chondrogenic marker expression to parental levels. |
RNAi silencing and overexpression in RCJ cell line; proliferation assays; proteoglycan/matrix production assays; RT-PCR for chondrogenic markers; rescue experiment |
Bone |
High |
19410023
|
| 2010 |
Mustn1 is an essential regulator of myogenic differentiation and myofusion. RNAi silencing of Mustn1 in C2C12 myoblasts did not affect proliferation but severely impaired myofusion and differentiation: silenced cells remained mononucleated and elongated poorly, with significant reductions in myogenin (Myog) and myosin heavy chain (Myhc) protein, and robust (~3-fold or greater) decreases in MyoD, desmin, and myofusion markers calpain 1 (Capn1), caveolin 3 (Cav3), and cadherin 15 (M-cadherin). MyoD and Myog are implicated as downstream targets of Mustn1. |
RNAi silencing in C2C12 myoblasts; immunocytochemistry; quantitative RT-PCR; morphological assessment of myotube formation |
American journal of physiology. Cell physiology |
High |
20130207
|
| 2012 |
Mustn1 is necessary for craniofacial chondrogenesis in vivo. Morpholino-mediated knockdown of Mustn1 in Xenopus laevis embryos produced craniofacial defects including small/absent eyes, shortened body axis, tail kinks, reduced cranial Sox9 mRNA, and loss of differentiated craniofacial cartilage (ceratohyal and pharyngeal arches). These effects were rescued by co-injection with morpholino-resistant Mustn1 mRNA, confirming specificity. |
Morpholino knockdown in Xenopus laevis; whole-mount in situ hybridization for Sox9; morphological scoring; mRNA rescue experiment |
Gene expression patterns |
High |
22281807
|
| 2013 |
Mustn1 promoter-driven GFP is expressed in activated satellite cells within 24 hours of activation but is absent in quiescent satellite cells. During skeletal muscle regeneration, Mustn1 expression precedes desmin expression and overlaps with MyoD (early) and myogenin (later), consistent with Mustn1 being upstream of desmin in regenerating muscle. |
Transgenic GFP reporter mice (Mustn1 promoter driving GFP); live imaging and immunofluorescence of regenerating muscle after cardiotoxin injury; single myofiber isolation; satellite cell activation assays |
Acta physiologica |
Medium |
23506283
|
| 2021 |
In chicken skeletal muscle satellite cells (SMSCs), MUSTN1 knockdown downregulated proliferation genes (Pax7, CDK-2) and differentiation genes (MyoD, MyoG, MyHC, MyH1B), upregulated apoptosis marker Caspase-3, reduced cell viability and EdU-positive cells, and increased G0/G1 phase while decreasing G2/M phase population. Conversely, MUSTN1 overexpression showed opposite effects on cell cycle distribution. |
siRNA knockdown and overexpression in chicken SMSCs; CCK-8 viability assay; EdU proliferation assay; flow cytometry cell cycle analysis; RT-qPCR for marker genes |
Experimental cell research |
Medium |
34536390
|
| 2023 |
Conditional knockout of Mustn1 in Pax7-positive skeletal muscle satellite cells in male mice results in increased glucose tolerance at 2 months of age, associated with upregulated GLUT1 and GLUT10 transporter mRNA expression and increased MUP-1, with decreased OSTN. These differences were absent at 4 months and were not observed in female KO mice, indicating a sex- and age-restricted link between Mustn1 and glucose homeostasis. |
Conditional knockout mouse (Pax7-Cre); intraperitoneal glucose tolerance test (IPGTT); RT-qPCR for metabolic genes |
Physiological reports |
Medium |
37170065
|
| 2023 |
Conditional knockout of Mustn1 in Pax7-positive satellite cells in mice results in altered skeletal muscle contractile function (20–50% decrease in isometric contraction force and 10–20% greater fatigue in soleus), and a shift in muscle fiber type composition: up to 15-fold increase in Type IIb fibers and ~20–30% decrease in Type I fibers, without gross morphological changes or significant alterations in myogenic differentiation/fusion gene expression. |
Conditional knockout mouse; ex vivo isometric contraction measurements; grip strength testing; gait analysis; immunofluorescence for fiber type markers |
FASEB bioAdvances |
Medium |
38094159
|
| 2024 |
Mustn1 is secreted from smooth muscle cells into the muscle extracellular space (present in arterioles of muscle microvasculature and muscle extracellular fluid), in addition to its previously reported intracellular/nuclear localization. Mustn1-deficient mice show altered extracellular matrix composition in skeletal muscle, and female Mustn1-deficient mice display higher collagen content after chemically induced muscle injury compared to wild-type littermates. |
Immunohistochemistry; bulk and single-cell RNA sequencing; extracellular fluid proteomics; Mustn1-deficient genetic mouse models; transcriptomics and proteomics of skeletal muscle and aorta |
Molecular metabolism |
Medium |
38458566
|
| 2025 |
MUSTN1 interacts directly with SMPX (Small Muscle Protein X-linked); SMPX's promotion of myogenic differentiation depends on MUSTN1. MUSTN1 stabilizes SMPX protein and maintains myofiber morphology. MUSTN1 knockout mice exhibit reduced muscle mass, decreased fiber cross-sectional area, reduced exercise endurance, and delayed muscle regeneration. |
Co-immunoprecipitation/protein interaction assays to identify SMPX as MUSTN1-interacting partner; MUSTN1 KO mice; muscle mass and fiber CSA measurements; exercise endurance testing; muscle regeneration assays |
Cell proliferation |
Medium |
39828423
|
| 2025 |
MUSTN1 interacts directly with FABP3 (Fatty Acid Binding Protein 3) and promotes preadipocyte proliferation and adipogenic differentiation via activation of the PI3K/AKT signaling pathway. MUSTN1 KO mice are protected against high-fat diet-induced obesity, hepatic steatosis, and insulin resistance. |
Protein interaction assays identifying FABP3 as MUSTN1 binding partner; MUSTN1 KO mouse on HFD; adipogenic differentiation assays in porcine and mouse preadipocytes; PI3K/AKT pathway analysis |
Journal of lipid research |
Medium |
40239869
|
| 2026 |
MUSTN1 is transcriptionally regulated by MyoD1. MUSTN1 directly binds to ACO1 (IRP1), enhancing ACO1's interaction with the 3' UTR of TFRC, thereby promoting TFRC expression and inhibiting SLC39A14, which reduces iron accumulation and lipid peroxidation (ferroptosis suppression). MUSTN1 is secreted via exosomes, and exosomal MUSTN1 promotes myoblast proliferation and differentiation while regulating ferroptosis. MUSTN1 mitigates dexamethasone-induced muscle atrophy. |
Transcriptome analysis; overexpression experiments; co-immunoprecipitation (MUSTN1-ACO1 interaction); RNA-binding assays (ACO1-TFRC 3'UTR); exosome isolation and treatment; functional assays for myotube area, proliferation, mitochondrial membrane potential; ferroptosis markers |
International journal of biological macromolecules |
Medium |
41547500
|
| 2026 |
MUSTN1 binds to STIMATE and impairs STIMATE's role in store-operated Ca2+ entry (SOCE): overexpression of the STIMATE-mustn1 fusion protein reduces SOCE compared to STIMATE alone. Overexpression of mustn1 alone does not alter SOCE. STIMATE-mustn1 overexpression does not change the cell cycle of MEG-01 cells (unlike STIMATE alone, which arrests cells in G2 phase). The STIMATE-mustn1 fusion protein shows different intracellular localization compared to STIMATE alone. |
Overexpression of STIMATE, mustn1, and STIMATE-mustn1 in MEG-01 and HEK293 cells; calcium imaging/SOCE measurement; confocal microscopy for co-localization of Orai1/STIM1; cell cycle analysis by flow cytometry |
FASEB journal |
Medium |
41677464
|