Sox3, affinity purified antibody, goat, 100 ug.
- Known as:
- Sox3, antigenic enriched (anti-), caprine, 100 ug.
- Catalog number:
- GT15119-100
- Product Quantity:
- 1
- Category:
- -
- Supplier:
- Neuromi
- Gene target:
- Sox3 affinity purified antibody goat 100 .
Ask about this productRelated genes to: Sox3, affinity purified antibody, goat, 100 ug.
- 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, affinity purified antibody, goat, 100 ug.
Related articles to: Sox3, affinity purified antibody, goat, 100 ug.
- Isolated growth hormone deficiency (IGHD) involves multiple genes, yet characterization of its mutational landscape and genotype-phenotype correlations remains limited. The aim of this study is to analyze a large cohort of patients with genetic IGHD and describe associated genotypes and phenotypes. - Source: PubMed
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Lima-Santos JúliaNascimento-Vidoti Carolina GamaCorreia-Costa Gabriela RoldãoCampos Nilma Lúcia ViguettiGuaragna Mara Sanchesde Oliveira Flávia MarcorinBarros Beatriz AmstaldenMiranda Marcio LopesAntolini Tavares ArthurGuerra-Junior GilMaciel-Guerra Andréa TrevasFabbri-Scallet HelenaVieira Társis Paiva - Postpartum depression (PPD) is a common and serious mental disorder after childbirth, imposing a heavy burden on mothers, infants, and families. Abnormalities in the tryptophan-kynurenine (TRP-KYN) metabolic pathway are considered to be involved in its pathogenesis, but the role of quinolinic acid phosphoribosyltransferase (QPRT), a key downstream enzyme in this pathway, remains unclear. This study aims to explore the association between PPD in women undergoing cesarean section and gene polymorphisms, as well as other risk factors for PPD. - Source: PubMed
Zhao ShanshanLin GuoxinLi ZiyuanPing AnqiWang SaiyingDuan Kaiming - SOX3 is a single-exon gene located on the X chromosome (Xq27.1), encoding a transcription factor critical for early central nervous system and pituitary development, as well as gonadal function. A growing body of literature reports a diverse array of phenotypes associated with different classes of SOX3 variants, including single nucleotide variants, indels, polyalanine tract changes, copy number variants, and structural rearrangements. These variants have been implicated in conditions ranging from pan-hypopituitarism or isolated growth hormone deficiency to neural tube defects, disorders/differences in sex development, and complex syndromes involving craniofacial and intellectual disability. In this review, we comprehensively summarize all known variants involving SOX3 reported to date, highlighting the different pathogenetic mechanisms that have been reported or hypothesized (e.g., gene dosage, transcriptional regulation) and the phenotypes to which these variants are associated to. Special emphasis is placed on established genotype-phenotype correlations and the challenges in interpretation relevant to clinical diagnostics. This review aims to provide a reference framework for clinicians, researchers, and geneticists working with SOX3-related disorders. - Source: PubMed
Publication date: 2026/04/24
De Dominicis ChiaraBirtolo Maria FrancescaLania Andrea GTrivellin Giampaolo - 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
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