ACVR2 _ ACTRII _ ACVR2A Protein
- Known as:
- ACVR2 _ ACTRII _ ACVR2A Protein
- Catalog number:
- 10257-H02H
- Product Quantity:
- 200
- Category:
- -
- Supplier:
- Smart Serology
- Gene target:
- ACVR2 _ ACTRII ACVR2A Protein
Related genes to: ACVR2 _ ACTRII _ ACVR2A Protein
- Gene:
- ACVR2A NIH gene
- Name:
- activin A receptor type 2A
- Previous symbol:
- ACVR2
- Synonyms:
- ACTRII
- Chromosome:
- 2q22.3-q23.1
- Locus Type:
- gene with protein product
- Date approved:
- 1993-09-17
- Date modifiied:
- 2018-02-13
Related products to: ACVR2 _ ACTRII _ ACVR2A Protein
Related articles to: ACVR2 _ ACTRII _ ACVR2A Protein
- Although fusions are actionable targets for a wide array of solid tumors, treatment-relevant biomarkers are heterogeneous and remain incompletely characterized for real-world fusion-positive populations. This retrospective cohort study provides a detailed molecular characterization of functional fusions and identifies biomarker associations in a real-world pan-cancer population. - Source: PubMed
Publication date: 2026/03/24
Zhou JianuoZong QinglanSun RuijiaWang XiangleiHuang MengliYu Wenyan - Pulmonary arterial hypertension (PAH) is characterized by dysfunction and remodeling of the pulmonary artery endothelium and smooth muscle. In heritable PAH, heterozygous loss-of-function mutations in the type II Bone Morphogenetic Protein (BMP) receptor gene () are the most common genetic cause. However, the mechanisms by which reduced BMPR2 levels alter endothelial signaling to drive PAH pathogenesis remain incompletely understood. To determine how BMPR2 levels govern signaling output and endothelial functional responses, we modulated BMPR2 expression in human pulmonary artery endothelial cells (PAECs) and assessed ligand-dependent SMAD1/5/8 signaling, proliferation, and caspase-3/7 activity. We found that BMP9 and BMP10 robustly activated SMAD1/5/8 signaling and promoted proliferation in PAECs, whereas the other ligands in this panel did not elicit a comparable signaling or proliferative response under these assay conditions. A moderate (~50%) reduction in BMPR2 protein levels (an in vitro approximation of haploinsufficiency) attenuated BMP9/10-induced SMAD1/5/8 activation, abolished proliferative responses, and was associated with a modest increase in caspase-3/7 activity, consistent with caspase pathway activation and early stress/injury signaling. Under BMPR2-limiting conditions, BMP9/10 responses became sensitive to Activin type II receptor blockade by bimagrumab, consistent with a context-dependent contribution of Activin type II receptors. Conversely, BMPR2 overexpression enhanced BMP9/10-dependent SMAD signaling and proliferation. Together, these findings support a receptor-dosage model where physiological BMPR2 expression is required to sustain homeostatic BMP9/10 signaling in pulmonary artery endothelium. This framework provides a basis for interpreting context-dependent pathway effects in PAH. - Source: PubMed
Publication date: 2026/03/10
Chu Kit-YeeThamilselvan VijayalakshmiCrawford Amberly NYu Paul BMartinez-Hackert Erik - Colon cancer is genetically heterogeneous, necessitating standardized genomic analyses for cross-cohort comparisons. Although The Cancer Genome Atlas-colon adenocarcinoma (TCGA-COAD) is a widely used dataset, its comparability to other ethnically different populations remains unclear. This study systematically compares the genomic characteristics of TCGA-COAD and ChangKang, a Chinese colon cancer cohort, using an identical data processing pipeline to minimize methodologic biases. - Source: PubMed
Chang Hsin-YuHuang Chien-JungYeh Yi-ChenWang Yu-Chao - Somatic mutations, or genetic changes occurring in cells after conception, are widespread in healthy tissues but are conventionally viewed as signs of pre-cancer or simply a consequence of aging. However, an emerging body of work has shown that somatic mutations can drive or protect against disease, which could inspire novel therapeutic strategies. The unexpected depth of genetic diversity within individuals also provides a massive substrate for discovering mutant genes selected for by disease. For instance, mutant hematopoietic cells can exacerbate inflammatory disease, and mutant hepatocytes can protect against liver disease. This suggests that somatic mutations, whether maladaptive or beneficial, could provide crucial insights into disease mechanisms, history, and reversal strategies. Somatic genetics offers a powerful, complementary approach to traditional germline genetics, which has had an enormous impact on biomedicine and drug development. This review explores the factors that shape the landscape of somatic mosaicism and discusses somatic mutations that cause or protect from disease. We highlight how somatic mutations are becoming a key discovery engine for disease genetics, moving rapidly toward drug target identification and clinical translation. - Source: PubMed
Brunner Simon FMartincorena IñigoMannino GregoryFox Caroline SStratton Michael RRubens Jacob RCampbell Peter JZhu Hao - Dizziness/vertigo is a multifactorial neurological disorder with complex ge-netic and cellular bases, yet its molecular mechanisms remain unclear. Understanding how gene regulation contributes to dizziness/vertigo may reveal novel neurobiological and therapeutic insights. - Source: PubMed
Publication date: 2026/02/11
Shan DingduoLi ShuoZhang LiliBai JiaqiWang Henglin