Ask about this productRelated genes to: ALK5 antibody
- Gene:
- TGFBR1 NIH gene
- Name:
- transforming growth factor beta receptor 1
- Previous symbol:
- MSSE, ESS1
- Synonyms:
- ALK-5, ACVRLK4, ALK5, TBRI, TBR-i
- Chromosome:
- 9q22.33
- Locus Type:
- gene with protein product
- Date approved:
- 1993-09-30
- Date modifiied:
- 2018-01-05
Related products to: ALK5 antibody
Related articles to: ALK5 antibody
- To present a comprehensive analysis of ocular features observed in pediatric patients diagnosed with Loeys-Dietz syndrome (LDS). - Source: PubMed
Publication date: 2026/05/06
Alsarhani Waleed KAl Nabulsi ReemAlAli AlaaBuncic J RaymondVincent AjoyMendoza RobertoO'Connor ConstanceAli Asim - Rho-associated coiled-coil kinase 1 (ROCK1) and Transforming Growth Factor Beta Receptor 1 (TGFBR1) are pivotal mediators of epithelial-mesenchymal transition (EMT), cytoskeleton remodeling, cell adhesion, and cancer metastasis. Their simultaneous inhibition offers a promising therapeutic strategy to disrupt cancer metastasis. This study integrates machine learning (ML)-based predictive QSAR (Quantitative Structure Activity Relationship) modeling, structure-activity relationship (SAR) analysis, ML-based virtual screening to identify dual inhibitors targeting both ROCK1 and TGFBR1. Bioactivity data with SMILES representation of ROCK1 and TGFBR1 inhibitors were sourced from ChEMBL. Molecular descriptors and fingerprints (e.g., Morgan, AtomPairs2D, etc) were computed using RDKit and PaDEL to encode molecular properties. Analysis of chemical similarity using Tanimoto coefficients identified activity-cliff pairs of compounds with high structural similarity but significant activity differences. QSAR models were developed using individual and combined fingerprints, with additional strategies such as excluding activity cliff pairs and stratified sampling based on pIC quantiles. Predictive machine learning models, including Random Forest (RF), Gradient Boosting (GB), XGBoost (XGB), K-Nearest Neighbors (KNN), Support Vector Machines (SVM), and Ridge Regression (RR), demonstrated robust performance (R > 0.6). The best ROCK1 and TGFBR1 models (RF Regressor) were used to screen a library of 1,48,684 compounds, resulting in the identification of a Hit (2-(1H-1,3-benzodiazol-1-yl)-N-[3-(1H-pyrazol-4-yl)phenyl]propanamide) with predicted dual ROCK1 (pIC = 7.29) and TGFBR1 (pIC = 7.00) inhibitory activity. Further, docking and molecular dynamics simulations of the Hit showed strong and stable interaction with both the targets hinge region residues, suggesting potential dual target inhibition activity. - Source: PubMed
Publication date: 2026/04/28
Kalita BikashitaCoumar Mohane Selvaraj - Malignant melanoma is characterized by marked intratumoral heterogeneity and an immunosuppressive tumor microenvironment (TME), and resistance to immunotherapy remains common. We hypothesized that melanoma contains a poorly differentiated tumor subpopulation characterized by an ETV5-centered transcriptional program and TGF-β-associated intercellular crosstalk, which may contribute to malignant progression and immune evasion. EV-related signaling was explored as a potential, but unvalidated, component of this phenotype. - Source: PubMed
Publication date: 2026/04/16
Li HaiboZheng XinGong YueXi MengranSun HaoyuDing YantaoSun Qi - Diabetic wounds, particularly diabetic foot ulcers, represent a significant clinical challenge owing to impaired vascularization, persistent inflammation, and dysfunctional extracellular matrix remodeling. Although adipose-derived stem cells offer therapeutic potential, their heterogeneity and functional impairment within the diabetic microenvironment limit their efficacy. Using single-cell RNA sequencing of human adipose and diabetic wound tissues, we identified a distinct CCL2-expressing ADSC subpopulation that is enriched in obese individuals and exhibits elevated stemness, unique metabolic profiles, and enrichment in pathways related to ECM organization and tissue development. This subpopulation functions as a key communication node, engaging with fibroblasts, macrophages, and endothelial cells through ligand-receptor interactions such as CCL2-ACKR1, TGFB1-TGFBR1, and IL34-CSF1R. Exosomes secreted by these CCL2-positive ADSCs were found to be enriched in CCL2, TGFB1, and IL34. In a diabetic mouse wound model, CCL2-ADSC-derived exosomes significantly accelerated wound closure compared with conventional exosomes, promoting angiogenesis, collagen deposition, and M2-macrophage polarization while reducing pro-inflammatory cytokines. In vitro, these exosomes reversed high-glucose-induced suppression of endothelial cell proliferation, migration, and tube formation. Mechanistically, CCL2 carried by the exosomes activates the PI3K/AKT/mTOR/HIF-1α signaling axis in endothelial cells via ACKR1, an effect abolished by CCL2 neutralization or ACKR1 knockdown. Together, these results demonstrate that the CCL2-positive ADSC subpopulation exerts multi-cellular and multi-target therapeutic actions, and that exosomes derived from this subpopulation offer a potent cell-free strategy to enhance diabetic wound healing by improving vascularization, modulating immune responses, and supporting ECM remodeling. - Source: PubMed
Zhao SongyunChen WanyingLiu KaiboXie JiahengChen YanmingDai HaoLu ZhongqiuChen LongwangHe YucangYu HuaLi Liqun - Myostatin (GDF-8), a TGF-β family myokine, regulates skeletal muscle growth and systemic metabolism and influences pituitary development and hormone secretion. This review summarizes experimental, translational, and clinical data linking myostatin to pituitary biology, including recent mouse evidence identifying muscle-derived myostatin as an endocrine driver of FSH synthesis via activin-type II/TGFBR1 signaling, with human confirmation pending. We analyze how pituitary disorders - growth hormone deficiency, acromegaly, hypercortisolism, central thyroid disease, central hypogonadism, and hypopituitarism - modify myostatin signaling, contributing to sarcopenia, anabolic resistance, and metabolic dysfunction. Across these conditions, human evidence remains limited and confounded by assay heterogeneity and comorbidities, as circulating myostatin often fails to mirror intramuscular changes. We propose an evidence framework emphasizing standardized assays (mature vs latent forms), longitudinal clinical cohorts, and integration of hormonal and functional endpoints. Myostatin remains a promising yet unvalidated biomarker and therapeutic target in endocrine-related muscle disease. - Source: PubMed
Iglesias Pedro