SOX9 Control Peptide
- Known as:
- SOX9 Control Peptide
- Catalog number:
- AP11362CP-N
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- ACR
- Gene target:
- SOX9 Control Peptide
Related genes to: SOX9 Control Peptide
- 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 Control Peptide
Related articles to: SOX9 Control Peptide
- In individuals with a 46,XY karyotype, heterozygous genetic variants have been associated with autosomal dominant male-to-female sex reversal accompanied by campomelic dysplasia. This report describes a child with Pierre-Robin sequence, skeletal abnormalities, and 46,XY differences of sex development. Exome sequencing was first performed with noninformative results and no variants were detected in the gene. Because skeletal anomalies suggested campomelic dysplasia, karyotype analysis was obtained despite normal female external genitalia. The karyotype analysis revealed a 46,XY complement with a de novo translocation between chromosomes 5 and 17 [46,XY,t(5;17)(q22;q23.1)dn]. Genome sequencing and optical genome mapping characterized the precise translocation breakpoint upstream of the gene. Use of high-resolution techniques was crucial to identifying the relevant genetic variant and confirming the diagnosis. Ultimately, this case demonstrates the value of optical genome mapping in identifying a cryptic rearrangement affecting the regulatory elements that cannot be detected by exome sequencing, underscoring its utility in differences of sex development diagnosis. - Source: PubMed
Publication date: 2026/08/12
Daghsni MarwaGuo FenForsyth RaeLynnReyes-Múgica MiguelYatsenko Svetlana AWitchel Selma Feldman - Cirrhosis, accounting for 2.4% of global mortality in 2019, represents a leading cause of death in chronic liver disease. Hepatic encephalopathy (HE), a decompensated complication of cirrhosis, is associated with a median survival of only 0.92 years post-diagnosis. Current screening methods relying on neuropsychological tests (e.g., Psychometric Hepatic Encephalopathy Score, PHES) have limitations such as time-consuming procedures and subjective interpretation, potentially delaying diagnosis. To address this, we integrated four cirrhotic transcriptomic cohorts (GSE41919, GSE57193, GSE139602, and GSE15654) and employed an integrated algorithm (LASSO [Least Absolute Shrinkage and Selection Operator]-RFE [Recursive Feature Elimination]-random forest) to identify HE-specific biomarker genes. Ultimately, we developed an HE risk-prediction system centered on eight HE-specific marker genes, namely, , , , , , , and . Based on these genes, an XGBoost (eXtreme Gradient Boosting)-based HE risk stratification model was constructed, and SHAP (SHapley Additive exPlanations) analysis was further introduced to address the "black-box" limitation of conventional machine learning models and to improve the interpretability. The finalized eight-gene system enables accurate, efficient, and interpretable HE risk assessment in patients with cirrhosis. Functional characterization through gene set enrichment analysis and structural equation modeling further revealed that these marker genes converge on four interconnected biological processes, namely, metabolic homeostasis, synaptic and neural transmission, immune inflammatory signaling, and hepatic detoxification, which collectively reflect the gut-liver-brain axis disruption central to HE pathogenesis. This dual-model system, incorporating both cirrhosis progression and survival prognosis, provides a reliable and clinically applicable tool for early HE risk warning and stratification, reducing the limitations of traditional neuropsychological screening and offering a translational foundation for timely intervention and prognostic optimization in high-risk cirrhotic patients. - Source: PubMed
Publication date: 2026/08/01
Lan YuanfengZhao TianXu YingYe Haihong - Stromal vascular fraction (SVF), an uncultured adipose-derived cell population, exerts regenerative effects primarily through paracrine mechanisms. While local intratesticular injection of SVF alleviates busulfan-induced testicular injury, the intravenous route remains unexplored. This study investigated whether intravenous SVF administration could mitigate busulfan-induced spermatogenic impairment. Adult male Sprague-Dawley rats received busulfan (15 mg/kg, intraperitoneal) or vehicle; the busulfan + SVF group received 2 × 10 allogeneic SVF cells intravenously immediately after busulfan injection. Two weeks later, we evaluated sperm parameters, testicular histopathology (Johnsen's score, seminiferous tubule diameter, germinal epithelial thickness), and immunohistochemical expression of SOX9 (Sertoli cells), CYP11A1 (Leydig cells), and DDX4 (germ cells). Busulfan alone induced severe spermatogenic defects, including reduced sperm count and motility, increased abnormal morphology, marked histopathological damage, and decreased expression of SOX9, CYP11A1, and DDX4. In contrast, intravenous SVF treatment significantly improved sperm count, motility, and testicular architecture, and restored the expression of SOX9, CYP11A1, and DDX4 within two weeks. This is the first demonstration that intravenous SVF attenuates early busulfan-induced testicular injury, providing preliminary evidence for a rapid, culture-free approach as a less invasive alternative to local injection. However, longer follow-up and fertility studies are needed to confirm sustained spermatogenic restoration. - Source: PubMed
Publication date: 2026/08/05
Li TiantianLiu ZhuojieYang FengDing LinshuYuan QiujuSo Kwok-FaiZhang YanWu Wutian - is an economically important amphibian in Northeast China, valued for its medicinal oviduct (). However, the low proportion of females in artificial culture severely restricts industrial productivity. To elucidate the molecular mechanisms of hormone-induced sex reversal, based on our previous research results, we exposed tadpoles to 17β-estradiol (E) or testosterone propionate (TP). We then monitored gonadal histology, conducted multi-stage transcriptome sequencing, and validated key genes via qRT-PCR. The results show that induction treatment with 40 μg·L E and 80 μg·L TP resulted in 93.33% female and 100% male populations, respectively. Both hormones promoted germ cell proliferation at the undifferentiated stage and directed stable ovarian or testicular development without intersex abnormalities. Ovarian differentiation involved progressive multi-wave transcriptional reprogramming, whereas testicular differentiation exhibited a concentrated gene expression burst during gonadal maturation. Steroid hormone biosynthesis, Wnt, and PPAR pathways formed the core regulatory network. Three female-biased genes (, , ) and three male-biased genes (, , ) were identified, with their expression dynamics aligned with histological progression. This study defines the optimal parameters and molecular signatures of bidirectional sex reversal in . It provides a practical foundation for sex-control breeding and offers amphibian-based evidence for the conservation and plasticity of vertebrate sex determination. - Source: PubMed
Publication date: 2026/08/06
Fu HualinSun YanqiuSun YiwenMeng XiangyuXu WeiXu YuanDu Zhiheng - Urine-derived stem cells (USCs) represent an accessible and non-invasive cell source with reported chondrogenic differentiation potential. However, the cellular heterogeneity and transcriptional dynamics underlying USC differentiation remain incompletely understood, limiting their translational interpretation. - Source: PubMed
Publication date: 2026/08/12
Schulz AlexanderBrockmann Emily MZentgraf MiriamBaur Andreas SUebe SteffenEkici Arif BDedden MarkZundler SebastianThiel Christian T