Ask about this productRelated genes to: Twist1 antibody
- Gene:
- TWIST1 NIH gene
- Name:
- twist family bHLH transcription factor 1
- Previous symbol:
- ACS3, BPES3, TWIST, CRS
- Synonyms:
- SCS, H-twist, BPES2, bHLHa38, CRS1
- Chromosome:
- 7p21.1
- Locus Type:
- gene with protein product
- Date approved:
- 1997-07-01
- Date modifiied:
- 2016-10-05
Related products to: Twist1 antibody
Related articles to: Twist1 antibody
- Following injury, predisposition towards regenerative repair and away from degenerative remodeling is central to organismal health, yet the upstream determinants that instruct this fate choice remain poorly understood. Here, we identify mesothelial cell plasticity as a central determinant between regeneration and degeneration by comparing mouse models of pneumonectomy (PNX) versus chronic lung allograft dysfuncton(CLAD). While mesothelial cells expand in both settings, following PNX, these cells undergo differentiation through multiple transitional states, culminating in an inflammatory population that orchestrates monocyte recruitment and subsequent tissue regeneration. In contrast, in CLAD, mesothelial cells enrich in an extracellular matrix-enriched state that lacks pro-regenerative signaling capacity. Using single cell epigenomic profiling and in vivo genetics, we define a mesothelium-specific TWIST1-CCL2 axis that governs mesothelium plasticity and signaling, monocyte recruitment and lung regrowth. Together, these findings demonstrate that context-dependent reprogramming of a pleural population, known to protect organs, can be leveraged to drive regeneration. - Source: PubMed
Publication date: 2026/07/31
Sun XinXu LeChen KevinDash BarshaYao BingpengLi RongboWang XinganZhou ZiheYu VincentSalamon RebeccaBawa PushpinderGuo MinzheBorok ZeaKotton DarrellEickelberg OliverBueno Marta - Craniosynostosis is a common congenital disorder characterized by premature fusion of one or more cranial sutures, categorized into non-syndromic (NSCS) and syndromic craniosynostosis (SCS). SCS accounts for ∼30% of cases, often accompanied by severe clinical complications, with 20%-25% of patients lacking a clear molecular etiology. - Source: PubMed
Publication date: 2026/08/04
Huang YufengHuang LingyueHu LilinTan LiZhao PeiweiLuo SukunYu TingHu YanqiuHe YuanzhiDu HaoHe Xuelian - Non-small cell lung cancer (NSCLC) is a leading cause of cancer-related mortality worldwide. Cigarette smoke extract (CSE) is a major environmental factor driving NSCLC progression, yet the underlying molecular mechanisms remain incompletely understood. Protein arginine methyltransferase 6 (PRMT6) is implicated in various malignancies, including NSCLC, and epithelial-mesenchymal transition (EMT) contributes to metastasis and poor prognosis in this disease. However, the role of PRMT6 in CSE-induced NSCLC progression has not been elucidated. - Source: PubMed
Zhang YanwenChang XiaojingCao JieZhang JingZhao Haiyan - Interleukin-6 (IL-6) and twist family bHLH transcription factor 1 (TWIST1) are critical regulators of cancer progression, including in pancreatic ductal adenocarcinoma (PDAC), but how they dynamically interact remains unclear. Therefore, this study aimed to elucidate the interaction between IL-6 and TWIST1 and explore the underlying mechanisms involved in PDAC progression. - Source: PubMed
Publication date: 2026/06/24
Yu MiaoHuang EnlaiSu MingxinTian ZhenfengLi YaqingLin XingyiHu BingrongChen YintingOu Guangsheng - Stromal cell states are altered in active Crohn's disease (CD), but their origin and phenotypic stability are unknown. Using single-cell spatial transcriptomics, RNA sequencing and ATAC sequencing of ~2,500,000 cells, we map 18 distinct stromal cell states within their cellular and cytokine signaling environments in human full-thickness CD bowel. Inflammatory fibroblasts (IFs) reside in immune cell-rich mucosal ulcers and are induced through combinatorial cytokine exposure suppressing submucosal universal fibroblast programs. The IF state is stabilized through transcription factor (TF) activity of GLI3, TWIST1, ETV4, PRDM1 and RELB, and does not spontaneously revert; however, histone deacetylase inhibition destabilizes the IF state, preventing IF secretome-induced epithelial transmigration and activation of neutrophils. The IF open chromatin configuration is distinct from that of fibrotic contractile stroma, which populate adjoining immune-depleted submucosal fibrotic niches. These findings show that microenvironments in pathological tissue niches shape open chromatin configuration of stromal states that are amenable to modulation by epigenetic modifiers. - Source: PubMed
Publication date: 2026/08/12
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