SOX8 (aa 247 to 258)
- Known as:
- SOX8 (aa 247 258)
- Catalog number:
- Y213828
- Product Quantity:
- 200ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- SOX8 ( 247 258)
Related genes to: SOX8 (aa 247 to 258)
- Gene:
- AKR1C4 NIH gene
- Name:
- aldo-keto reductase family 1 member C4
- Previous symbol:
- CHDR
- Synonyms:
- DD4, HAKRA, C11, 3-alpha-HSD, CDR, MGC22581
- Chromosome:
- 10p15.1
- Locus Type:
- gene with protein product
- Date approved:
- 1993-08-26
- Date modifiied:
- 2016-06-03
- Gene:
- AKTIP NIH gene
- Name:
- AKT interacting protein
- Previous symbol:
- FTS
- Synonyms:
- FLJ13258
- Chromosome:
- 16q12.2
- Locus Type:
- gene with protein product
- Date approved:
- 2001-10-02
- Date modifiied:
- 2014-11-18
- Gene:
- ANKDD1A NIH gene
- Name:
- ankyrin repeat and death domain containing 1A
- Previous symbol:
- -
- Synonyms:
- FLJ25870
- Chromosome:
- 15q22.31
- Locus Type:
- gene with protein product
- Date approved:
- 2006-02-16
- Date modifiied:
- 2019-02-18
- Gene:
- ARHGAP19 NIH gene
- Name:
- Rho GTPase activating protein 19
- Previous symbol:
- -
- Synonyms:
- FLJ00194, MGC14258
- Chromosome:
- 10q24.1
- Locus Type:
- gene with protein product
- Date approved:
- 2003-12-05
- Date modifiied:
- 2016-10-05
- Gene:
- ARMC9 NIH gene
- Name:
- armadillo repeat containing 9
- Previous symbol:
- -
- Synonyms:
- FLJ12584, KIAA1868, ARM, KU-MEL-1
- Chromosome:
- 2q37.1
- Locus Type:
- gene with protein product
- Date approved:
- 2005-10-04
- Date modifiied:
- 2014-11-18
Related products to: SOX8 (aa 247 to 258)
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- Long non-coding RNAs (lncRNAs) are important regulators of complex traits in pigs and the systematic annotation and functional roles of these genes remain poorly understood. This study aimed to construct a comprehensive porcine lncRNA atlas and explore the regulatory role of lncRNAs in muscle development. - Source: PubMed
Publication date: 2026/07/27
Liu HangWang HaoWang LigangZhang YuedongGuo ChaoTao LinPeng MinshengZhou ZhongyinYang RuifeiZhang Yaping - Islr2 (Linx) is a transmembrane protein that mediates correct formation of the internal capsule/cerebral peduncle. Here, we have utilized a combination of transgenic reporter alleles and immunohistochemical markers to trace striatal direct pathway (Sox8-EGFP), corticofugal (Fezf2-tdTomato), and thalamocortical (Netrin-G1) trajectories throughout development in several different permutations of Islr2 conditional knockout (cKO) mice. Firstly, we used Isl1 to recombine Islr2 in the newborn direct pathway striatal projection neurons (dSPNs) as well as the corridor (Co) cells and thalamic reticular nucleus (TRN) and found this resulted in a complete loss of the internal capsule/cerebral peduncle including dSPN, corticofugal and thalamocortical axons. Despite the severe dSPN axon defects in these cKOs, the Co forms correctly. To examine a potential role for Islr2 in the TRN, which borders the axonal trajectories of the rostral internal capsule, we used Foxd1. These Islr2 cKOs showed no overt defects in dSPN, corticofugal or thalamocortical axons within the internal capsule/cerebral peduncle. Finally, to distinguish a role for Islr2 specifically in maturing SPNs versus newborn dSPNs and Co cells, we used Gpr88 and observed defasciculation and misrouting of dSPNs within the direct pathway. Importantly, these cKOs showed a notable reduction in corticofugal axons within the posterior internal capsule together with a loss of the cerebral peduncle while thalamocortical axons remained intact. Taken together, our results highlight a central role for Islr2 on dSPN axons for the correct assembly of the internal capsule/cerebral peduncle trajectories. - Source: PubMed
Publication date: 2026/07/04
Ali SaimaEhrman Jacqueline MMerchan-Sala PalomaMatthew Kofron JWaclaw Ronald RCampbell Kenneth - 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 - The development of resistance to anticancer therapies in cancer cell is a major challenge in the treatment of oral squamous cell carcinoma (OSCC), a common malignant tumor. Erythropoietin-producing hepatocellular A2 (EphA2) affects several cancers, and this study examined its role in enhancing OSCC. Following screening, EphA2 and SRY-Box transcription factor 8 (SOX8) knocked down and overexpression cell lines were constructed, followed by treatment with Cetuximab. Quantitative real-time polymerase chain reaction, western blot, cell counting kit-8, wound healing, and transwell assay were used to detect the relevant indicators. Co-immunoprecipitation was used to detect the interaction between EphA2 and SH2 domain-containing protein-tyrosine phosphatase-2 (SHP2). Double luciferase reporter gene experiment and chromatin immunoprecipitation experiment were performed to verify the regulatory mechanism of EphA2 and SOX8. The mouse tumor model was established, and the tumor development was observed after plasmid transfection and Cetuximab treatment. EphA2 was highly expressed in OSCC cells, and overexpression of EphA2 up-regulated SOX8. EphA2 regulated SOX8 and associated protein expression to increase OSCC cell migration and invasion. EphA2 knockdown made OSCC cells more sensitive to Cetuximab, whereas SOX8 overexpression reduced this sensitivity. We found SHP2 bound to SOX8. Down-regulation of EphA2 decreased tumor growth in mice, increased Cetuximab sensitivity, and overexpression of SOX8/SHP2 decreased Cetuximab sensitivity. OSCC had elevated EphA2 levels, which enhanced cell migration and invasion via SHP2/SOX8 and impaired Cetuximab sensitivity. Down-regulation of EphA2 decreased tumor growth and enhanced Cetuximab sensitivity, suggesting new OSCC targets and potential treatments. - Source: PubMed
Publication date: 2026/05/26
Yan DayongGuo LelePei FeiZhong Ketao - Non-small cell lung cancer (NSCLC) is the most common subtype of lung cancer, and the prognosis of NSCLC patients is still poor particularly for patients with metastatic disease. Thus, extending the knowledge about the mechanism of metastasis is critical for NSCLC treatment. We demonstrated that hsa_circ_0073052 (circPOLK) was overexpressed in blood exosomes from cancer patients than those from healthy people. CircPOLK overexpression enhanced the metastasis and EMT progression of NSCLC cells. Next, circPOLK might function as miRNA sponge in NSCLC cells. Through bioinformatical prediction and RNA pull-down experiment, miR-1204 might be a potential target of circPOLK. Interestingly, serumal miR-1204 was an efficacious diagnostic and prognostic molecular for lung cancer patients and acted as a suppressor on NSCLC progression. Furthermore, circPOLK promoted metastasis of NSCLC via regulating miR-1204. Furthermore, SOX8 was identified as a potential target of circPOLK/miR-1204. GO enrichment of circPOLK regulated DEGs showed that circPOLK might be involved in angiogenesis of NSCLC. Indeed, circPOLK secreted by NSCLC cells could promote angiogenesis. Our dada not only identifies a novel circPOLK/miR-1204/SOX8 signaling pathway, but also provides therapeutical strategies for NSCLC patients with metastatic disease. - Source: PubMed
Publication date: 2026/05/08
Li Yang-LingLiu Ye-HanCheng JingWei Zhen-QiangLin Neng-MingZhang Chong