SOX3 antibody - N-terminal region (ARP33321_P050)
- Known as:
- SOX3 (anti-) - N-terminal region (ARP33321_P050)
- Catalog number:
- arp33321_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- SOX3 antibody - N-terminal region (ARP33321_P050)
Related genes to: SOX3 antibody - N-terminal region (ARP33321_P050)
- Gene:
- SOX3 NIH gene
- Name:
- SRY-box 3
- Previous symbol:
- PHP
- Synonyms:
- -
- Chromosome:
- Xq27.1
- Locus Type:
- gene with protein product
- Date approved:
- 1993-11-30
- Date modifiied:
- 2015-11-23
Related products to: SOX3 antibody - N-terminal region (ARP33321_P050)
Related articles to: SOX3 antibody - N-terminal region (ARP33321_P050)
- Idiopathic non-obstructive azoospermia (iNOA) is associated with reduced expression of multiple eukaryotic translation initiation factors ( ) in spermatogonia, including eukaryotic translation initiation factor 5 ( ). The present study revealed that eIF5 mRNA and protein levels were markedly higher in male mouse ( ) germ cells than in Leydig or Sertoli cells. Thus, to define the role of eIF5 in spermatogenesis, conditional knockout (cKO) mice were generated by crossing mice with ( )-Cre mice. Loss of in male germ cells reduced both SRY-box transcription factor 3 (SOX3) progenitor spermatogonia and Kit proto-oncogene receptor tyrosine kinase (KIT) differentiating spermatogonia, leading to severe meiotic failure and complete male infertility. Mechanistically, deficiency impaired translation of genes involved in ubiquitination, autophagy, and DNA repair, which, in turn, triggered excessive endoplasmic reticulum (ER) stress and compromised DNA repair in SOX3 progenitor spermatogonia. These defects promoted DNA damage and subsequent apoptosis, resulting in progressive germ cell depletion and sterility. Collectively, these findings highlight the essential role of eIF5 in spermatogenesis and offer a potential therapeutic strategy for iNOA associated with reduced expression of and other translation initiation factors. - Source: PubMed
Wei HongweiHuang YatingWang WeiyongLiu ShuangLiu HuiyuChu HanyuSun Yan-LiDu YanLi WenqianZhang LuchunWeng YashuangZhang WenboZhang MeijiaWang Zhijuan - Foxg1 is a transcription factor that plays important roles in the development of the nervous and sensory systems. In the olfactory epithelium, it is known that Foxg1 is necessary for the development of subsets of olfactory sensory neurons, though its precise role remains undefined. In this study, we show that in zebrafish Foxg1a is required for the formation of microvillous olfactory sensory neurons, as well as regulation of subsets of sensory neurons and progenitor cells in the embryonic olfactory epithelium. Using the foxg1a zebrafish line, we found that sox10 and trpc2b expression are both absent from the olfactory epithelium in these mutants, suggesting that there are defects in the development of microvillous olfactory sensory neurons. Another major class of olfactory sensory neurons in the olfactory epithelium, ciliated cells, appear to develop normally in foxg1a mutants. Additional groups of neurons, such as Islet1-positive sensory neurons and mechanosensory rod cells are decreased but not absent in foxg1a mutant embryos. Progenitor cell populations in the olfactory epithelia are differentially affected, with an increase in the number of Sox2-positive cells and a decrease in Sox3-positive and Pax6-positive cells in foxg1a mutant embryos as compared to heterozygous sibling controls. Finally, we show that foxg1 embryos do not form olfactory epithelium neuron projections to the brain. These results show a nuanced role for Foxg1 in the developing olfactory epithelium. - Source: PubMed
Publication date: 2026/03/19
Christian Sarah KLiwaru LaylahIbrahim NusaybahReddy DivyaVanderbeck MadisonHendricks Roe CMcGraw Hillary F - This narrative review summarises glioblastoma (GBM), a very frequent invasive kind of brain tumour in the elderly that is extremely aggressive, resistant to treatment, and has a bad prognosis because of its substantial genetic and cellular heterogeneity. With a median survival of about 15 months, GBM is still an incurable cancer. This review takes full 3 months for collect all relevant knowledge about PAX and SOX gene families, which have crucial roles in the biology of GBM, as shown by recent developments in molecular pathology. Depending on certain gene expression patterns, members of these transcription factor families have been shown to have both oncogenic and tumor suppressive properties. They are important regulators of brain development, stem cell maintenance, and tumor progression. While PAX6 functions as a tumor suppressor, preventing growth and angiogenesis, PAX3, PAX5, and PAX8 are increased in GBM, encouraging proliferation, stemness, and survival. Similarly, SOX7 and SOX11 act as suppressors, and their downregulation is associated with malignancy and a bad prognosis, while SOX2, SOX3, SOX4, and SOX9 increase tumor aggressiveness and resistance to treatment. Glioma cell migration, growth, and death inhibition are further fueled through the complex interactions between canonical and non-canonical WNT signaling that modulate PAX and SOX pathways. These results highlight how crucial thorough molecular profiling is for improved categorization, prognostication, and the creation of focused treatment plans in GBM. The discovery of the dual functions of the PAX and SOX genes in GBM highlights their potential as therapeutic targets and biomarkers, opening up new possibilities for more individualised and accurate treatment approaches. - Source: PubMed
Publication date: 2026/03/03
Polley KallolFirdous Sayed Mohammed - We established a 3D model of human NT2/D1-derived early neural progenitor cells immobilised in alginate microfibres as a system for testing the neurotoxicity of energy drinks and their components, either alone, together, or in combination with alcohol. The system supports the retinoic acid-induced neurogenesis of NT2/D1 cells, and the proliferative capacity of the NT2/D1-derived early neural progenitor cells was maintained in the 3D environment. Cell cycle distribution and the expression of pluripotency markers (, and ), early neural markers (, and ), and (a marker of neural commitment), showed profiles characteristic of early neural progenitors. Treatments with an energy drink and its major components (caffeine and taurine) - either alone, together, or in combination with alcohol - had different effects on the proliferative capacity of the NT2/D1-derived early neural progenitor cells in the 2D and 3D models. In the 2D-cultured cells, all treatments except for caffeine led to a significant decrease, while cells within the 3D model exhibited a significant increase after treatment with caffeine, or after combined treatment with energy drink and alcohol. Preliminary findings suggesting that there were no treatment effects on OCT4 and PAX6 protein expression in either model, should be further confirmed. This human cell-based 3D model could potentially represent a rapid and cost-effective system for assessing the acute and long-term neurotoxicity of various compounds. - Source: PubMed
Publication date: 2026/02/24
Pejić JelenaMilivojevic MilenaSchwirtlich MarijaBojic LukaStojkovska JasminaPetrovic IsidoraStevanovic MilenaMojsin Marija - Structural variants (SVs) may increase SOX3 expression in the gonads and have been observed in individuals with ovotesticular differences in sex development (OT-DSD) and XX testicular differences in sex development (T-DSD). Most of the SVs found in OT-DSD individuals are whole-gene duplications, and to date, only one SV affecting SOX3 expression by a positional effect has been described. We report an individual raised as a female with SRY-negative OT-DSD. Karyotype analysis showed a pericentric inversion in one of the X chromosomes - 46,X, inv(X)(p22;q27). The breakpoints and fusion were mapped using optical genome mapping (OGM) and short-read whole genome sequencing. One of the breakpoints was mapped on Xq27.1 (genomic position chrX:140,420,874 - GRCh38), 82 kb downstream of the SOX3 gene. This breakpoint was predicted to interrupt a topological associate domain (TAD) affecting 24 enhancer-promoter interactions of SOX3. RNA sequencing (RNA-seq) of a formalin-fixed paraffin-embedded (FFPE) sample of the gonads confirmed increased SOX3 expression. The present study is the first to analyze gene expression in gonadal tissues from an OT-DSD individual, and the first reporting an inversion-based mechanism leading to XX OT-DSD. Additionally, an X-inactivation assay on DNA extracted from the gonads revealed random inactivation. These findings support the hypothesis that inappropriate SOX3 expression may result from the positional effects of SVs, leading to OT-DSD in 46,XX individuals. - Source: PubMed
Publication date: 2026/02/12
Nascimento-Vidoti Carolina GamaFabbri-Scallet HelenaGuaragna Mara Sanchesde Wallau Melissa Bittencourtde Souza Vanessa Sodréda Costa Silvia SouzaKrepischi Ana Cristina VictorinoMazzeu Juliana ForteCarvalho Claudia M BMaciel-Guerra Andréa TrevasGuerra-Júnior GilVieira Társis Paiva