SOX9 antigen
- Known as:
- SOX9 antigenic
- Catalog number:
- 'H00006662-P01-10
- Product Quantity:
- 10
- Category:
- -
- Supplier:
- ACR
- Gene target:
- SOX9 antigen
Related genes to: SOX9 antigen
- Gene:
- SOX9 NIH gene
- Name:
- SRY-box 9
- Previous symbol:
- CMD1, CMPD1
- Synonyms:
- SRA1
- Chromosome:
- 17q24.3
- Locus Type:
- gene with protein product
- Date approved:
- 1992-09-25
- Date modifiied:
- 2018-06-25
Related products to: SOX9 antigen
'F 4_80 Antigen (mouse) Host Rat'F 4_80 Antigen (mouse) Host Rat(Anti_Tg)Thyroglobulin Antigen(Des-Asp187)-Melanocyte Protein PMEL 17 (185-193) (human, bovine, mouse)
(Des-Asp187)-ME20M_ME20S (185-193) (human, bovine, mouse), (Des-Asp187)-Melanocyte Lineage-Specific Antigen GP100 (185-193) (hu(Des-Asp187,Met186)-Melanocyte Protein PMEL 17 (185-193) (human, bovine, mouse)
(Des-Asp187,Met186)-Melanoma-Associated ME20 Antigen (185-193) (human, bovine, mouse), (Des-Asp187,Met186)-95 kDa Melano(Des_Asp187,Met186)_Melanocyte Protein PMEL 17 (185_193) (human, bovine, mouse) Salt Trifluoroacetate Binding _ Synonym (Des_Asp187,Met186)_Melanoma_Associated ME20 Antigen (185_193) (human, bovine(Des_Asp187,Met186)_Melanocyte Protein PMEL 17 (185_193) (human, bovine, mouse) Salt Trifluoroacetate Binding _ Synonym (Des_Asp187,Met186)_Melanoma_Associated ME20 Antigen (185_193) (human, bovine(Des_Asp187,Met186)_Melanocyte Protein PMEL 17 (185_193) (human, bovine, mouse) Salt Trifluoroacetate Binding _ Synonym (Des_Asp187,Met186)_Melanoma_Associated ME20 Antigen (185_193) (human, bovine(Des_Asp187,Met186)_Melanocyte Protein PMEL 17 (185_193) (human, bovine, mouse) Salt Trifluoroacetate Binding _ Synonym (Des_Asp187,Met186)_Melanoma_Associated ME20 Antigen (185_193) (human, bovine(Draxin) C1ORf187, Antigen blocking peptide(Val438)-Tyrosinase (432-444) (human)
(Val438)-LB24-AB (432-444) (human), (Val438)-Monophenol Monooxygenase (432-444) (human), (Val438)-SK29-AB (432-444) (human), (Val438)-Tumor Rejection Antigen AB (0x19 Antigen0x2 Antigen1,25-dihydroxyvitamin D3 Competitive ELISA, Coated with Antigen105 kDa islet cell antigen,BEM-3,Brain-enriched membrane-associated protein tyrosine phosphatase,ICA105,PTP IA-2,PTPLP,Ptprn,Rat,Rattus norvegicus,Receptor-type tyrosine-protein phosphatase-like N,R-P Related articles to: SOX9 antigen
- Background Disorders/differences of sex development (DSDs) comprise a group of congenital conditions characterized by atypical gonadal and/or anatomical development of the reproductive system. Among them, XX DSD (SRY-negative) represents a rare but clinically relevant condition, defined by the presence of testicular or ovotesticular tissue in chromosomal females lacking the SRY gene. This phenotype has been described in humans and several domestic species, including dogs, cats, and goats. Summary Over the past decades, studies in dogs with 78,XX DSD (SRY-negative) have primarily focused on identifying causative mutations in candidate genes, particularly in SOX9. However, only a limited number of cases have been associated with SOX9 copy number variations, suggesting that additional genetic factors remain to be identified. In contrast, FOXL2, a key regulator of ovarian development and maintenance, has been relatively underexplored in canine studies. Functional evidence from mouse models highlights the importance of FOXL2 in ovarian differentiation and maintenance, as well as in craniofacial and skeletal development. 78,XX DSD has been increasingly reported in French Bulldogs, a breed predisposed to craniofacial and ocular abnormalities. Key Messages Current evidence indicates that FOXL2 is a biologically plausible candidate gene for 78,XX DSD in dogs, although no causative variants have yet been identified. The observed cryptic relatedness among affected French Bulldogs suggests a shared genetic background. Future studies should include comprehensive sequencing of FOXL2, particularly its GC-rich coding regions, together with detailed clinical phenotyping. Integrating molecular and clinical data may improve understanding of the genetic basis of XX DSD and support more informed breeding strategies. - Source: PubMed
Publication date: 2026/07/04
Krzeminska Paulina - Astrocytes are the most common glial cells in the mammalian central nervous system. Their diverse structures and functions, along with their critical role as key regulators of brain activity, have recently gained recognition. However, the lack of specific cell markers makes it difficult to identify particular subpopulations. In this study, we examined the distribution of traditional astrocyte markers-glial fibrillary acidic protein (GFAP), SRY-box9 (SOX9), and S100 protein beta (S100β)-in the adult mouse brain. In the cerebral cortex, striatum, and thalamus, most cells did not express GFAP, with limited overlap between GFAP and either SOX9 or S100β. In contrast, the pons-medulla showed a higher rate of co-expression of GFAP and SOX9 compared to the cerebral cortex. In the hippocampus, GFAP was widely expressed and showed significant overlap with SOX9 and S100β. Co-staining of SOX9 and S100β was frequently observed in the cerebral cortex, striatum, thalamus, and midbrain, and S100β-positive cells were more common than SOX9-positive cells. These results reveal regional differences in astrocyte marker expression, highlight the limitations of relying on a single marker like GFAP, and underscore the importance of using multiple markers. - Source: PubMed
Publication date: 2026/06/24
Kawaguchi YukinoTerashima YuriTanaka SatoshiOkuda Hiroaki - In this study, we developed a gelatin methacryloyl (GelMA) hydrogel composite for the simultaneous delivery of glucosamine (GlcN), platelet-rich plasma (PRP), and bone marrow-derived mesenchymal stem cells (BMMSCs). We systematically investigated its effects on cartilage endplate (CEP) cell behavior, inflammation, and oxidative stress, and evaluated its reparative efficacy in a murine caudal CEP injury model. - Source: PubMed
Publication date: 2026/06/15
Bao YinghaoHu BaoyangBai YangZhang YingMeng HanluWang HeFang Fang - CDK4 alterations are common in lung adenocarcinoma, but recent clinical trials only demonstrated modest therapeutic responses to CDK4/6 inhibitors. The mechanism of CDK4/6 inhibitor resistance has not been fully characterized. - Source: PubMed
Publication date: 2026/06/27
Cheung Alvin Ho KwanWong Kit YeeLi Gordon Yuan-HoXie FudaWu QiuqiuYuen Thomas Tin HoHui Pak LamHuang PingmeiLiu XiaoliChen BonanJi FenfenDong YujuanCheng Alfred Sze-LokNg Calvin Sze HangZhang XiangWong Chi ChunYu JunKang WeiTo Ka-Fai - In mammalian sex differentiation, Sox9 expression in undifferentiated gonads determines male development. Sox9 is regulated by multiple enhancers, of which Enh13/mXYSRa is the most critical. Disruption of the GATA4 binding site in Enh13/mXYSRa causes XY sex reversal in the C57BL/6J (B6J) strain, but not in the mixed genetic background of B6J × DBA/2. To clarify the cause of these differences, mice with the same mutation were generated in DBA/2. Homozygous mutants developed as XY males. We hypothesized that the phenotypic differences between strains were due to functional differences of another enhancer. Mice lacking TESCO and carrying a mutation in the GATA4 binding site were generated and analyzed. The mutants developed according to their chromosomal sex despite reduced Sox9 expression. These findings imply that the DBA/2 genetic background contains factors preventing Sox9 expression from falling below the threshold required for male development. Bulk RNA-seq analysis of fetal gonads during sex determination identified strain-dependent differences in intermediate mesoderm development and protease inhibition pathways; the study also revealed that the expression of Sox8 has a redundant role in Sertoli cell differentiation to that of Sox9 in male embryonic gonads. These differences may contribute to the phenotypic variation observed between strains. - Source: PubMed
Tsuchiya IkuTsuji-Hosokawa AtsumiFuruhashi SuzuneSugiyama KarinOgawa YuyaOishi AkiTerao MihoTakada Shuji