Ask about this productRelated genes to: HAND1 antibody
- Gene:
- HAND1 NIH gene
- Name:
- heart and neural crest derivatives expressed 1
- Previous symbol:
- -
- Synonyms:
- eHand, Thing1, Hxt, bHLHa27
- Chromosome:
- 5q33.2
- Locus Type:
- gene with protein product
- Date approved:
- 1999-05-17
- Date modifiied:
- 2016-10-05
Related products to: HAND1 antibody
Related articles to: HAND1 antibody
- Atrial septal defect (ASD) is a common congenital heart disease (CHD) and genetic variation in the HAND1 gene is associated with cardiac development. The variants in the promoter region of the HAND1 gene are unknown. - Source: PubMed
Publication date: 2026/04/30
Qi Jia-LeChen Huan-XinHou Hai-TaoYang QinHe Guo-Wei - Long-term exposure to low-dose food contact materials (FCMs) has raised concerns regarding developmental toxicity. In the present study, we prioritized FCMs with potential developmental toxicity using a weight-of-evidence computational model, which predicted 127 chemicals to be of high concern. From these, we selected 7 chemicals-representing both high and low concern categories-and evaluated their potential embryotoxicity using the mouse embryonic stem cell test (mEST). Among the selected chemicals, thiram most strongly inhibited cardiac differentiation in mEST. We further examined the effects of thiram on morphology and expression of differentiation-related genes in mouse embryonic stem cells (mESCs). Treatment with thiram inhibited 50% early differentiation in mESCs, suppressed the expression of markers associated with the three-germ layers, but increased the expression of neurectoderm markers during early embryogenesis. Additionally, treatment with 20 ng/mL thiram, which was the lowest-observed-effect concentration of cytotoxicity, disrupted neuronal differentiation in both mESCs and human pluripotent embryonal carcinoma NT2 cells. Finally, based on transcriptome analysis, 20 and 30 ng/mL thiram disrupted the neural crest differentiation pathway, altering the expression of genes including homeobox A1 (HOXA1), homeobox B1 (HOXB1), Heart And Neural Crest Derivatives Expressed 1 (HAND1), Distal-Less Homeobox 5 (DLX5), and transcription factor AP-2 alpha (TFAP2A) in NT2 cells. Therefore, disruption of neural crest differentiation is one of the potential mechanisms underlying thiram-induced embryotoxicity. The integrated alternative approach adopted in the present study to identify mechanism-based biomarkers for thiram-induced embryotoxicity in a human-relevant model could facilitate safety assessment for data-poor chemicals in future. - Source: PubMed
Publication date: 2026/04/21
Ho Chia-ChiTung Chun-WeiYen B LinjuWeng Chen-YiHsu Ju-HsinTsai Ming-HsienArrokhman SalimLin Pinpin - Trophoblast and amniotic lineages, representing key extra-embryonic tissues, can be differentiated from human pluripotent stem cells (hPSCs) under chemically defined conditions. However, the regulatory mechanisms coordinating the fate decision between these lineages during PSC differentiation remain incompletely understood. Leveraging CRISPR/Cas9-mediated loss-of-function screening in lineage-reporter PSCs, we identified the transcription factor HAND1 as a critical determinant controlling the bifurcation of trophoblast and amniotic lineages. Genetic ablation of HAND1 effectively abrogated the amniotic differentiation capacity of PSCs while concomitantly enhancing their trophoblast differentiation potential. Conversely, ectopic HAND1 overexpression impaired trophoblast differentiation. Notably, forced HAND1 expression in human trophoblast stem cells (TSCs) induced transcriptional reprogramming toward an amniotic fate, indicating its lineage-instructive capability. Mechanistic analyses demonstrated that HAND1 interacts with the TCFs and Wnt signaling effectors β-catenin to form a transcriptional complex that antagonistically modulates the balance between trophoblast- and amnion-associated gene regulatory networks. Collectively, our findings establish HAND1 as a master regulator orchestrating the amniotic versus trophoblast lineage choice during human PSC differentiation, thereby illuminating fundamental regulatory mechanism underlying extra-embryonic lineage specification. - Source: PubMed
Publication date: 2026/03/10
Pang ChangmiaoYang QifengZhong YulongYe JinhaoLv YufangXie ShufeiTang YanqingYe XianhuaZhang FeifanLi ChaoZhang JingyiSun LiangzhongAi ShanshanGao Xuefei - Long tails trigger tail biting in pigs and increase the risk of flystrike infections in sheep. Tail docking has been a common management practice in both species for decades, but increasingly conflicts with legal animal welfare guidelines. Sustainable solutions require breeding strategies targeting shorter tails. In consequence, the aims were to conduct whole-genome sequencing (WGS)-based genome-wide association studies (GWAS) and comparative genomic analyses (CGA) to explore functional elements influencing tail traits. Phenotypically divergent experimental populations of pigs and sheep were established through unified selection and mating experiments. Tail traits included tail length (TL) measured at birth, and tail abnormalities (TA) assessed radiographically at 14 weeks of age. WGS-based GWAS identified a significant locus on SSC18 in pigs and suggestive loci for TL in both species, which, together with previously reported loci for TA, were further analyzed by CGA. The genomic windows of the significant locus on SSC18 in pigs and the TL GWAS locus on OAR4 in sheep were found to be conserved, harboring six common genes with predicted functional variants. These variants were jointly associated with TL (Plm < 0.05) in both species in linear regression models adjusted for sex, age of the dam, body length, and body weight. In other GWAS locus windows (±1 Mb), species-specific TL candidate genes were identified in sheep (HOXB13, MUC5B, EPB41L3, MTCL1, PIEZO2, MPPE1, and LOXHD1) and in pigs (KNL1, DISP2, SPRED1, TGFB2, and HAND1), each harboring associated putative functional variants. For TA, sheep-specific candidates (PGM2, LRRC66, CRACD, LOC105601916, and SH2D4B) and pig-specific candidates (MYOT, TMCO6, and PCDHAC2) were revealed using logistic regression models (Pglm < 0.05). GO analyses of candidate genes predicted shared biological processes between sheep and pigs, whereas pathway analyses indicated that common carbohydrate metabolism pathways, along with species-specific immune and inflammatory signaling, and pig-specific TGF-β signaling and endochondral ossification, may contribute to tail length variation and abnormalities. These findings provided deeper insights into the genetic basis of differential embryonic tail morphogenesis and perinatal tail development across species. - Source: PubMed
Publication date: 2026/03/03
Zhang XuyingMainzer JohannaGiambra IsabellaYin TongEngel PetraHümmelchen HannahWagner HenrikWehrend AxelEgerer ChristianeGerhards KatharinaReiner GeraldKönig Sven - Chronic Obstructive Pulmonary Disease (COPD) is a progressive inflammatory lung disorder influenced by environmental and genetic factors. The rs3741240 polymorphism in the gene, which encodes the anti-inflammatory protein CC16, is considered a genetic marker of COPD susceptibility. - Source: PubMed
Publication date: 2025/12/12
Sultana NasimaAdhikari HimaniGoswami Achintya MohanMondal AmaleshGanai IndranilBiswas HimaniIqbal AsifDas AratrikaMoitra SaibalPodder Sanjoy