Ask about this productRelated genes to: Hmx3 antibody
- Gene:
- HMX3 NIH gene
- Name:
- H6 family homeobox 3
- Previous symbol:
- -
- Synonyms:
- NKX5-1
- Chromosome:
- 10q26.13
- Locus Type:
- gene with protein product
- Date approved:
- 1995-01-20
- Date modifiied:
- 2018-11-16
Related products to: Hmx3 antibody
Related articles to: Hmx3 antibody
- Social isolation, characterized by a lack of social connections with family, friends, and others, is associated with adverse health outcomes. However, the genetic contribution to the susceptibility to social isolation remains unclear. This study aimed to identify genetic loci associated with social isolation using the Lubben Social Network Scale (LSNS-6) in a Japanese population. The Tohoku Medical Megabank Community-Based Cohort Study was conducted between 2013 and 2016. The participants were genotyped using the Affymetrix Axiom Japonica Array. The LSNS-6 was used to assess familial and friend ties through six questions and social isolation statuses were defined using the total scale, family subscale, and friend subscale. Genome-wide association studies (GWASs) were conducted using a generalized linear mixed model, adjusting for age, sex, 10 genetic principal components and batch effects. In total, 63,497 participants who completed genotyping and the LSNS-6 were included. The mean age was 59.4 ± 11.9 years, and 41,126 (64.8%) were female. Significant genetic loci were identified in GWASs for the total scale (rs10736933 near ACADSB and HMX3) and friend subscale of LSNS-6 (rs1778366 near LINC02315 and LRFN5). This study provides the first genome-wide evidence of social isolation in the Japanese population, suggesting associations with ACADSB, HMX3, LINC02315, and LRFN5. These findings could enable personalized prevention and intervention for social isolation and related psychiatric disorders. - Source: PubMed
Publication date: 2026/02/17
Ohseto HisashiInoue KosukeTakahashi IppeiObara TakuNarita AkiraIshikuro MamiOrui MasatsuguMurakami KeikoNoda AoiShinoda GenkiTakase MasatoNakaya NaokiKogure ManaHatanaka RiekoNakaya KumiChiba IppeiTokioka SayuriKotozaki YukaShimizu AtsushiTanno KozoHozawa AtsushiTamiya GenKondo NaokiKuriyama Shinichi - Endochondral ossification is a physiological process involving a sequential formation of cartilage and bone tissues. Classically, cartilage and bone formation have been considered independent processes at cellular level. However, the recently described multiple cell differentiation dynamics suggest that some bone cells are indeed the progeny of cartilage cells, or chondrocyte-derived osteoblasts. We hypothesized that the cartilage-to-bone phenotype transition is triggered by specific molecular events. First, the process was assessed in mouse bone tissue, and then, it was mimicked using in vivo cell implantation and in vitro serial differentiation protocols. Data indicates that cartilage cells transition to bone cell phenotype during postnatal physiological bone formation. This process can be reproduced using cartilage precursor cells coupled to specific implantation procedures or differentiation protocols. Gene expression profiling reveals that NOTCH, BMP and MAPK signaling pathways are relevant at the phenotype-switch, while the transcription factors Mesp1, Alx1, Grhl3 and Hmx3 are the feasible driver genes for chondrocyte-derived osteoblasts formation. Altogether, this report shows that endochondral ossification can be modeled using primary cell cultures and data indicate that this process is regulated by specific molecular events, previously described at skeleton morphogenesis during embryo development, and from now on also linkable to postnatal bone development and regeneration processes. - Source: PubMed
Publication date: 2026/02/09
Ruiz-Hernández RaquelGay LaurieMoncho-Amor VerónicaMartín PabloVergara-Arce Jhonatan ADi Blasio StefaniaSnoeks ThomasCossío UnaiMatheu AnderCaffarel Maria MGerovska DanielaAraúzo-Bravo Marcos JVilas AmaiaProsper FelipeMoya SergioAlonso-Alconada DanielAlonso-Varona AnaNusspaumer GretelLopez-Rios JavierRizotti KarineLovell-Badge RobinBonnet DominiqueMalanchi IlariaAbarrategi Ander - Hmx2 was required for type B intercalated cell differentiation but became dispensable in the absence of Dmrt2. Dmrt2 promoted type A differentiation of intercalated cells and repressed type B identity. Early divergence of Dmrt2 and Hmx2 marked subtype specification of intercalated cells. - Source: PubMed
Publication date: 2025/10/06
Feng YuQi YanmiaoYang YangAlexander Stephen IXia YinZheng Xiangjian - Intercalated cells (ICs) in the mammalian kidney regulate circulatory pH through IC subtype-restricted actions of bicarbonate transporters: pH is elevated by Slc4a1 restricted to type A-ICs (A-ICs) and depressed by Slc26a4 in type B-IC (B-ICs). NonA-nonB-ICs (nA/nB-ICs) also produce Slc26a4 though their function is unclear. Though both nephron and ureteric progenitor lineages generate A-ICs, the former also generates nA/nB-ICs and the latter B-ICs. Lineage and cell type restricted transporter gene expression in the mouse and human kidney is preceded by expression of the transcriptional regulators in A-ICs, and either, or both, and in B- and nA/nB ICs. CRISPR/Cas9-directed removal of and the linked / resulted in IC-subtype switching. A-ICs adopted an B-IC cell fate on Dmrt2 removal while B-ICs initiated a Dmrt2/Slc4a1 A-IC program on removal. Triple knockout of , , and resulted in hybrid ICs expressing both and . Thus, restricted expression of these regulators is essential for specifying IC subtypes. To explore these mechanisms, and were activated ectopically in ureteric organoid cultures. Introduction of -a pan determinant of ICs-activated early A-IC development while cointroduction of silenced Foxi1-dependent expression and led to an upregulation of Slc26a4. In contrast, coexpression of and upregulated . These data support a model in which mutually repressive interactions between and establish distinct IC identities and ongoing activity of these factors supports gene regulatory programs specific to each IC subtype. - Source: PubMed
Publication date: 2025/05/12
Parvez Riana KKim Doh KyungCsipán Réka LGuo JinjinZeng ZipengZhang Chennan CLi ZhongweiMcMahon Andrew P - KMT2A::MLLT3 acute myelomonocytic leukemia (AML) comes in two clinically and biologically different subtypes. One is characterized by inferior outcome, older age, and MECOM oncogene expression. The other is mainly observed in children and young adults, associates with better clinical outcome, but lacks MECOM. To identify cell fate determining transcription factors downstream of KMT2A::MLLT3, we applied a bioinformatic algorithm that integrates gene and enhancer expression from primary MECOM-positive and -negative KMT2A::MLLT3 AML samples. This identified MECOM to be most influential in the MECOM-positive group, while neuronal transcription factor HMX3 was most influential in the MECOM-negative group. In large AML cohorts, HMX3 expression associated with a unique gene expression profile, younger age (p < 0.002) and KMT2A-rearranged and KAT6A-CREBBP leukemia (p < 0.00001). HMX3 was not expressed in other major genetic risk groups and healthy blood cells. RNA-sequencing analyses following forced HMX3 expression in healthy CD34+ cells and its silencing in KMT2A::MLT3 cells showed that HMX3 drives cancer-associated E2F and MYC gene programs (p < 0.001). HMX3 expression in healthy CD34+ cells blocked monocytic but not granulocytic colony formation. Strikingly, HMX3 silencing in KMT2A::MLLT3 patient cells resulted in cell cycle arrest, monocytic differentiation and apoptosis. Thus, the neuronal transcription factor HMX3 is a leukemia-specific vulnerability in KMT2A::MLLT3 AML. - Source: PubMed
Publication date: 2024/12/04
Arza-Apalategi SaioaHeuts Branco M HBergevoet Saskia MMeering RoosGilissen DaanJansen Pascal W T CKrippner-Heidenreich AnjaValk Peter J MVermeulen MichielHeidenreich OlafHaferlach TorstenJansen Joop HMartens Joost H Avan der Reijden Bert A