Twist1 antibody - N-terminal region (ARP37996_P050)
- Known as:
- Twist1 (anti-) - N-terminal region (ARP37996_P050)
- Catalog number:
- arp37996_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- Twist1 antibody - N-terminal region (ARP37996_P050)
Related genes to: Twist1 antibody - N-terminal region (ARP37996_P050)
- 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 - N-terminal region (ARP37996_P050)
Related articles to: Twist1 antibody - N-terminal region (ARP37996_P050)
- Airway hyperresponsiveness (AHR) is a clinically important feature of chronic pediatric inflammatory airway disease, but its cellular architecture remains incompletely resolved. Because bulk transcriptomic approaches can mask signals from rare or state-specific cell populations, single-cell RNA sequencing (scRNA-seq) offers a useful framework for examining epithelial and immune cell diversity in hyperresponsive airways. - Source: PubMed
Publication date: 2026/06/09
Yang WeimingMao ShunfengZhou Liuyang - Following the publication of the above paper, it was drawn to the Editor's attention by a concerned reader that the β‑actin control blots featured in Fig. 7C on p. 8 had already appeared previously in an article written by different authors at different research institutes that was also published in the journal . Owing to the fact that the contentious data in the above article had already been published prior to its submission to , the Editor has decided that this paper should be retracted from the Journal. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a reply. The Editor apologizes to the readership for any inconvenience caused. [Molecular Medicine Reports 24: 592, 2021; DOI: 10.3892/mmr.2021.12231]. - Source: PubMed
Publication date: 2026/06/11
Tao MeiZheng DannaLiang XudongWu DiandianHu KangJin JuanHe Qiang - The genetic basis of impaired intestinal barrier function in preterm infants is poorly understood. Variants in single immunoglobulin interleukin-1-related receptor (SIGIRR), a negative regulator of Toll-Like Receptor (TLR) signaling, have been identified in preterm infants with necrotizing enterocolitis (NEC). We hypothesized that SIGIRR variants associated with NEC impair gut barrier function to pathobionts. To determine how SIGIRR genetic variants disrupt neonatal intestinal barrier integrity and promote susceptibility to Gram-negative bacteria implicated in sepsis and NEC pathogenesis. - Source: PubMed
Publication date: 2026/06/04
Venkatraman AparnaYu WeiMenden Heather LMabry Sherry MWheatley Joshua LUmar ShahidChavez-Bueno SusanaSampath Venkatesh - Pulmonary fibrosis (PF) is a progressive interstitial lung disease with poor prognosis and limited therapeutic options, largely due to the lack of physiologically relevant and dynamically traceable preclinical models. Here, we establish an induced pluripotent stem cell (iPSC)-derived alveolar organoid platform that faithfully recapitulates PF-like remodeling upon TGFβ1 stimulation. The organoids exhibit lineage commitment to the distal lung epithelium (NKX2.1, SFTPC/SFTPB) and, following TGFβ1 exposure, undergo hallmark fibrotic changes including organoid condensation and size reduction, collagen deposition (Masson's trichrome), myofibroblast activation (α-SMA), up-regulation of profibrotic genes (COL1A1, FN, VIM, ACTA2), and partial EMT-like reprogramming (↑CDH2, TWIST1, and ↓CDH1). To enable label-free, longitudinal readouts, we integrate a deep neural network (YOLOv8-nano) that detects subtle morphological cues directly from bright-field images and classifies treatment status with high fidelity. Across augmented datasets (8892 images), the model achieved strong performance on the original context-preserving images (mAP50-95 up to 0.95; high precision/recall and 98-99% true-positive rates), supporting robust discrimination of control versus TGFβ1-treated organoids. This AI-enhanced organoid system provides a quantitative, label-free platform for monitoring fibrotic remodeling and offers a scalable foundation for preclinical antifibrotic screening and mechanism-of-action studies. - Source: PubMed
Publication date: 2026/05/07
Kim Seung HyeonLee JooyeonHan Jong HyeokSeo Sang HyukJang JiminLee Jong-HeeHong Seok-HoJu Myeong JinLee Dae-HeeJeon Hee-JaeYang Se-Ran - DLGAP5 is frequently upregulated in human cancers and is associated with tumor progression. However, its biological role, regulatory mechanism, and downstream signaling in lung adenocarcinoma (LUAD) remain unclear. - Source: PubMed
Publication date: 2026/05/28
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