SOX1 antibody - C-terminal region (ARP34352_P050)
- Known as:
- SOX1 (anti-) - C-terminal region (ARP34352_P050)
- Catalog number:
- arp34352_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- SOX1 antibody - C-terminal region (ARP34352_P050)
Related genes to: SOX1 antibody - C-terminal region (ARP34352_P050)
- Gene:
- SOX1 NIH gene
- Name:
- SRY-box 1
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 13q34
- Locus Type:
- gene with protein product
- Date approved:
- 1993-11-30
- Date modifiied:
- 2015-11-23
Related products to: SOX1 antibody - C-terminal region (ARP34352_P050)
Related articles to: SOX1 antibody - C-terminal region (ARP34352_P050)
- Posterior axis development during mammalian embryogenesis is driven by transient progenitor states that give rise to neural and mesodermal lineages, including neuromesodermal progenitors (NMPs). In vitro derivation of posterior progenitor populations from human pluripotent stem cells (hPSCs) has relied on modulation of Wnt and FGF signaling; however, these approaches frequently generate heterogeneous and unstable cell populations. Here, we investigated whether sodium butyrate (NaB) supplementation could promote a posteriorly biased intermediate state without extensive extracellular signaling control. We show that NaB, a histone deacetylase inhibitor, promotes the induction of posterior pre-neural progenitors (PNPs) characterized by co-expression of CDX2 and SOX2, together with suppression of SOX1. Transcriptomic analyses revealed that NaB-treated cells exhibit a posteriorly enriched PNPs with restrained anterior neural differentiation, transient early induction, and progressive activation of posterior genes, consistent with an incompletely caudalized intermediate rather than a fully specified NMP population. Importantly, these PNPs remained responsive to canonical neural tube patterning cues, including retinoic acid and smoothened agonists, enabling further differentiation toward ventral spinal cord lineages. Collectively, our findings demonstrate that NaB supplementation supports posterior PNPs from hPSCs, providing a simple and reproducible platform for modeling early posterior neural development in vitro. - Source: PubMed
Publication date: 2026/07/22
Oh Kyung TaekKim Deok HoHong WonjunPark KyoungminYou HakyoungLee Cheol-KooOh ChulhongPark Gun-HooYou Seungkwon - Paraneoplastic autoimmune encephalitis (PAE) is most commonly associated with small cell lung cancer (SCLC). Anti--aminobutyric acid B receptor (GABABR) antibodies underlie a treatable limbic syndrome, whereas anti-SRY-box transcription factor 1 (SOX1) antibodies serve as high-specificity onconeural biomarkers of SCLC-driven autoimmunity. The sequential emergence of these two antibodies during the longitudinal course of a single patient has rarely been documented. - Source: PubMed
Publication date: 2026/07/09
Liu FengJiang Ye-HanHu Yu-FangQin Jin-GuanLiu Guang-Sheng - Long non-coding RNAs (lncRNAs) are increasingly recognized as regulators of brain cell function, but their roles in astrocyte biology and neurodegeneration remain poorly understood. Here, we identify as a conserved, brain-enriched lncRNA that is downregulated in Alzheimer's disease and in reactive astrocyte states. Antisense oligonucleotide-mediated depletion of in astrocytes revealed a transcriptional program marked by activation of p53 target genes selectively associated with cell-cycle inhibitory pathways. Consistent with this, depletion enhanced p53 occupancy at target promoters such as , increased expression and levels of its protein product p21, and thereby induced G1 arrest and reduced astrocyte proliferation. In contrast, other canonical p53 outputs, including apoptosis and senescence, were not affected, indicating that selectively modulates distinct branches of p53 signaling. Notably, loss of was accompanied by impaired glutamate uptake, reduced lactate secretion, and altered astrocyte support functions, suggesting that these deficits arise as downstream consequences of the p53-dependent transcriptional shift rather than direct primary effects of loss. Together, these findings identify as an astrocyte-enriched regulatory layer that constrains a p53-dependent cell-cycle program and highlight its role in shaping astrocyte state transitions in Alzheimer's disease. - Source: PubMed
Publication date: 2026/07/03
Fuchs UlrikeSchröder SophiePena TonatiuhKrüger Dennis MBurkhardt SusanneSchütz Anna-LenaHempel NinaGisa VerenaTaghavi TarannomCortes JonathanGertig MichaelDelalle IvanaSananbenesi FarahnazFischer André - Lambert-Eaton myasthenic syndrome (LEMS) is a rare autoimmune disorder characterized by impaired acetylcholine release at the neuromuscular junction, leading to proximal muscle weakness, autonomic dysfunction, and diminished or absent tendon reflexes. Here, we present a rare case of a 73-year-old male smoker with small cell lung cancer (SCLC), whose initial manifestation was LEMS. Notably, the patient tested seronegative for anti-voltage-gated calcium channel (VGCC) antibodies but was seropositive for anti-SOX1 antibodies. The diagnosis of LEMS was supported by characteristic clinical symptoms and electromyography findings. Subsequent imaging (chest CT and PET-CT) identified a left upper lobe lung mass, which was pathologically confirmed as SCLC, clinically staged as T1cN3M0 (IIIB). Following standard antitumor therapy, the patient's muscle weakness markedly improved, and his overall survival has exceeded 36 months. This case underscores the critical importance of testing for anti-SOX1 antibodies and applying the DELTA-P score for malignancy screening in high-risk patients presenting with LEMS-like symptoms, even when seronegative for anti-VGCC antibodies. - Source: PubMed
Publication date: 2026/06/17
Chen YezhouZhang JianHou QinglunLi HenLiu JieShi WenhuiSun Meili - To evaluate clinical performance of FAM19A4, SOX1, and PAX1 methylation testing as a triage method for women ≥30 with positive non-16/18 high-risk HPV (hrHPV). - Source: PubMed
Publication date: 2026/06/23
Feng PeiyuShi KeyiZhao WeiZhang JijunChen XiaoZhu JunChen GangWang ZhiqiZhou XinZhou FengCheng XiaodongLi Yang