LHX1 antibody - C-terminal region (P100851_T100)
- Known as:
- LHX1 (anti-) - C-terminal region (P100851_T100)
- Catalog number:
- p100851_t100
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- LHX1 antibody - C-terminal region (P100851_T100)
Related genes to: LHX1 antibody - C-terminal region (P100851_T100)
- Gene:
- LHX1 NIH gene
- Name:
- LIM homeobox 1
- Previous symbol:
- -
- Synonyms:
- LIM-1, LIM1
- Chromosome:
- 17q12
- Locus Type:
- gene with protein product
- Date approved:
- 1996-10-02
- Date modifiied:
- 2015-09-03
Related products to: LHX1 antibody - C-terminal region (P100851_T100)
Related articles to: LHX1 antibody - C-terminal region (P100851_T100)
- Aging of the male reproductive system is characterized by declining fertility, with epididymal dysfunction being a critical yet poorly understood contributor. Through a multimodal analysis in non-human primates that integrated histology and transcriptomics, we delineated a coherent epididymal aging phenotype encompassing epithelial senescence, chronic inflammation, fibrosis, and functional decline. Single-nucleus transcriptomics revealed principal cells (PCs) as the predominant and most transcriptionally perturbed epithelial cell type. Within PCs, the longevity-associated transcription factor FOXO1 was markedly downregulated with age. Functional studies in human epididymal epithelial cells demonstrated that FOXO1 deficiency drives cellular senescence. Mechanistically, FOXO1 transcriptionally activates LHX1, and this axis is essential for counteracting senescence. Furthermore, intervention with senescence-resistant mesenchymal progenitor cells or their exosomes mitigated epididymal aging phenotypes and restored FOXO1 expression in vivo and in vitro. Our study establishes the FOXO1-LHX1 axis as a key protective pathway against primate epididymal aging, providing mechanistic insights and potential therapeutic targets for preserving male reproductive health. - Source: PubMed
Publication date: 2026/03/24
Lu HuifenCai LinguoLv DongLiangSun GuoqiangLei JinghuiNing TaixinXin ZijuanHuang HaoyanJing YingHuang DaoyuanSun ShuhuiMa ShuaiZhang WeiqiGao FeiChen RuiQin YingyingSong WeihongXiang Andy PengIzpisua Belmonte Juan CarlosLiu Guang-HuiQu JingWang Si - - Source: PubMed
Chen Chih-Ping - The suprachiasmatic nucleus (SCN) is considered the master pacemaker of the circadian clock in mammals, but our current knowledge of the SCN is mostly based on rodent studies. Here, we report a comprehensive molecular and cellular atlas for the adult human SCN by spatial transcriptomics, single-nucleus RNA sequencing, and deep-learning-based histological analysis. We identified seven human SCN neuron subtypes with specific transcriptomes and spatial distributions. Comparison of humans, mice, and non-human primates revealed the conserved functional segregation within the SCN regulated by LIM homeobox 1 (LHX1) and RAR-related orphan receptor B (RORB). Furthermore, our results suggested that the human SCN has undergone marked reorganization of its neuropeptide signaling network. Finally, integrative analysis of human SCN transcriptomes and genome-wide association studies (GWASs) identified arginine vasopressin (AVP)/neuromedin S (NMS) subtype as the potential neuronal correlate for morningness chronotype. Thus, our spatial and single-cell transcriptomic atlas of the human SCN provided a basis for the understanding of neural and molecular mechanisms of the human circadian clock. - Source: PubMed
Publication date: 2026/02/19
Yang QiaoqiaoWang HaifangGao LeMa DanyiXiong YangyangTian YeLiu YiwenShen ZhimingZhang XiaobiaoLi WenshengYan Jun - Among the disorders of sex development (DSD) with karyotype 46,XY, there is a group of diseases caused by defects of androgen synthesis. The last stage of in the synthesis of androgens is the conversion of testosterone into a more active androgen dihydrotestosterone, which occurs under the influence of the enzyme 5α-reductase type II (SRD5A2). SRD5A2 deficiency is a rare disease with autosomal recessive inheritance. - Source: PubMed
Publication date: 2025/12/02
Kalinchenko N YMakretskaya N AKolodkina A AKareva M ATiulpakov A N - Inherited renal hypomagnesemia is rare but may indicate an underlying genetic condition, and it should be considered when evaluating unexplained hypomagnesemia. 17q12 deletion syndrome, a recurrent microdeletion including HNF1B (hepatocyte nuclear factor 1 beta) and neighboring genes such as LHX1 (LIM homeobox 1) and ACACA (acetyl-CoA carboxylase alpha), is associated with renal magnesium wasting, neurodevelopmental deficits, and multi-organ involvement. However, spinal cord anomalies, particularly syringomyelia, have not been reported to date. - Source: PubMed
Publication date: 2025/12/24
Özdemir Atikel YeşimKocaağa AyçaDelil Kenanİskender Mazman DuyguÇakır Meltem DidemYimenicioğlu Sevgi