Ask about this productRelated genes to: STX1A antibody
- Gene:
- STX1A NIH gene
- Name:
- syntaxin 1A
- Previous symbol:
- STX1
- Synonyms:
- HPC-1, p35-1
- Chromosome:
- 7q11.23
- Locus Type:
- gene with protein product
- Date approved:
- 1992-09-09
- Date modifiied:
- 2016-10-05
Related products to: STX1A antibody
Related articles to: STX1A antibody
- Syntaxin1A (STX1A) is a presynaptic membrane protein that is abundantly expressed in the central nervous system. It is a key member of the soluble N-ethylmaleimide sensitive factor attachment protein receptor protein family. Notably, STX1A acts as a 'molecular hub' in neural networks by regulating presynaptic membrane fusion with synaptic vesicles and the subsequent release of neurotransmitters. In addition to this function, STX1A is crucial for neuronal development, synaptic plasticity, and ion channel regulation. The deficiency or variation of not only directly disrupts neurotransmitter transmission but also contributes to pathological processes in neurological disorders such as Alzheimer's disease, epilepsy, autism spectrum disorder, and ischemic stroke by interfering with excitatory-inhibitory balance, inducing neuroinflammation, and triggering neuronal apoptosis. The present review summarizes the structure and physiological functions of STX1A, highlights its mechanisms in the pathogenesis of various neurological diseases, and examines its potential as a diagnostic biomarker and therapeutic target for these diseases. - Source: PubMed
Publication date: 2026/03/26
Huang YatingXi JunSu BaolingWang PeipeiXie CuimeiYuan YifanYin XiaopingBao Bing - Retinal diseases (RDs) involve the degeneration of retinal cells, particularly retinal ganglion cells (RGCs), often driven by glutamate imbalance and aberrant signaling. We previously identified a presynaptic self-amplifying mechanism of glutamate overflow, where NMDA overstimulation activates JNK2-mediated phosphorylation of STX1A. To block this mechanism, a cell-permeable peptide, called JGRi1, was previously developed to disrupt the JNK2-STX1A interaction. Here, we investigated whether the inhibition of this pathway by JGRi1 could provide neuroprotection in retinal degeneration. We showed that JGRi1 efficiently reached the mouse retina upon topical administration as eye drops and granted retinal protection. Using an ex vivo optic nerve cut (evONC) model, we demonstrated that JGRi1 preserved RGC viability, reduced phosphorylation of JNK and STX1A, and lowered glutamate release. In retinal wholemounts, JGRi1 similarly preserved RGC survival. Furthermore, in an NMDA-induced degeneration model, JGRi1 protected RGCs, reduced glutamate levels, disrupted the JNK2-STX1A interaction, and limited microglial infiltration. Collectively, our findings highlight the central role of the JNK2-STX1A pathway in retinal degeneration and identify JGRi1 as a promising neuroprotective tool. - Source: PubMed
Publication date: 2026/04/15
Cimino MarcoSerkiz JackKonstantopoulos Joanne KTisi AnnamariaCappelletti PamelaMaccarrone RitaSappington Rebecca MFeligioni Marco - Williams syndrome (WS; OMIM #194,050) is a multisystem pediatric genetic disorder caused by a heterozygous microdeletion of a 1.5-1.8 Mb region at chromosome 7q11.23, encompassing 26 to 28 genes. Clinical hallmarks include cardiovascular anomalies, distinctive craniofacial morphology and neurodevelopmental deficits characterized by hypersociability, cognitive impairment and anxiety. Although causative therapies for WS still remain elusive, advances in gene editing and forebrain organoids have already greatly furthered our understanding of the underlying mechanisms. - Source: PubMed
Publication date: 2026/03/17
Chen Ya-YueChen Wei-JunZhang RuiJi ChaiZhang Yu-HanMa Da-QingShi Qiao-JuanXie Yi-Cheng - Shiga toxin-producing Escherichia coli (STEC) is a zoonotic pathogen and a common cause of foodborne infection. The stx genes are the main virulence factors and are classified into different subtypes. Some subtypes are more associated with severe infections than others, i.e. the HUS-associated stx. Other virulence factors, such as eae, are also commonly observed, particularly from severe infections. Ruminants, in particular cattle, are recognized as the main reservoir for STEC; however, STEC is also isolated from pigs. In the present study, minced beef and pork were analyzed for STEC using two different approaches. Minced beef was analyzed for STEC of specific serogroups (O26, O91, O103, O121, O145, and O157), while for minced pork, all STECs were of interest. A specific real-time PCR screening for stx was also employed. In total, 308 samples of minced beef and 157 of minced pork were collected and analyzed using ISO TS 13136:2012. After screening of minced beef, 28 samples met the criteria for isolation and STEC was isolated from two samples. Furthermore, after screening for and isolation of potentially stx-positive STEC, STEC was isolated from two more samples. The isolates were characterized by whole genome sequencing as STEC O26:H11 (stx, eae), O91:H21 (stx), O22:H8 (stx, stx), and O178:H19 (stx, stx). This suggests that the occurrence of STEC in minced beef is most likely underestimated when only looking for STEC of specific serogroups. While 46 of 157 samples were positive for stx and/or stx in the screening of minced pork, STEC was not isolated from any of the samples. No samples were positive for stx. While the occurrence of STEC of the specific serogroups in minced beef is low, it is difficult to draw any firm conclusions about the occurrence of STEC in minced pork. The results highlight the issue with PCR-positive/culture-negative results as observed for both sample types. - Source: PubMed
Publication date: 2026/03/12
Johannessen G SUrdahl A MJohansen A MBækken M SØkland MSekse C - Williams-Beuren Syndrome (WBS), a neurodevelopmental disorder caused by a heterozygous microdeletion at chromosome 7q11.23, is characterized by hypersociability and enhanced affective empathy. However, the specific genetic and neural mechanisms within the WBS locus underlying this elevated empathic response remain unknown. Here, we investigated empathy-related behaviors, including observational fear and allogrooming, in WBS mouse models harboring a deletion within the conserved syntenic region on mouse chromosome 5. We demonstrate that WBS mice exhibited emotional contagion and prosocial consolation behaviors comparable to their wild-type controls. Furthermore, WBS mice with single-gene deletions of the cortex-enriched genes Abhd11, Limk1, Mlxipl, and Stx1a also showed unaffected empathic freezing behavior. Collectively, our findings suggest that the enhanced empathic responsiveness reported in individuals with WBS may be influenced by reduced social inhibition toward others, while acknowledging that limitations of current rodent behavioral assays preclude definitive conclusions regarding primary neural mechanisms of empathy. - Source: PubMed
Publication date: 2026/03/11
So DahmCha Hye LimLee SuaKim SowonYoo EunsuKeum Sehoon