Caspr2, affinity purified antibody, sheep, 100 ug.
- Known as:
- Caspr2, antigenic enriched (anti-), ovine, 100 ug.
- Catalog number:
- SP15104-100
- Category:
- -
- Supplier:
- Neuromi
- Gene target:
- Caspr2 affinity purified antibody sheep 100 .
Related genes to: Caspr2, affinity purified antibody, sheep, 100 ug.
- Gene:
- CNTNAP2 NIH gene
- Name:
- contactin associated protein like 2
- Previous symbol:
- -
- Synonyms:
- Caspr2, KIAA0868, NRXN4
- Chromosome:
- 7q35-q36.1
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-01
- Date modifiied:
- 2019-04-09
Related products to: Caspr2, affinity purified antibody, sheep, 100 ug.
Related articles to: Caspr2, affinity purified antibody, sheep, 100 ug.
- KCNA1 encodes the α-subunit of the voltage-gated potassium channel KV1.1. Mutations in KV1.1's pore domain result in developmental and epileptic encephalopathy (DEE), where early life seizures and a culprit lesion synergistically disrupt neurodevelopmental trajectories, resulting in intellectual disability that often presents with disturbances in sleep, sociability and sensory processing. Abnormalities in the subcellular localization of Kv1.1, via mutations in/autoantibodies against LGI1 and CNTNAP2, also give rise to syndromes of epilepsy and neuropsychiatric impairment. Mice with deletions of Kcna1("-/-") are known to display spontaneous seizures at 2-3 weeks of age and premature mortality. In this study, we applied instrumented home-cage monitoring to examine how aberrations in KCNA1 expression may result in pervasive alterations in spontaneous behavior. Compared to wildtype, Kcna1-/- mice displayed a robust multifaceted behavioral syndrome featuring marked nocturnal hyperactivity, reduced sleep and sheltering, fragmented feeding/drinking rhythms, abnormal sensory responsivity and diminished wheel-running. In similar recordings, Kcna1+/- mice only displayed increased sheltering, Lgi1+/- mice displayed mild sleep reductions and Cntnap2-/- mice showed home-cage hypoactivity. Kcna1 loss in parvalbumin-positive interneurons (PV-Cre) resulted in a subtle phenocopy, with mild reductions in sleep accompanied by reduced sheltering behavior, while Kcna1 deletions in forebrain pyramidal neurons (Emx1-Cre) or dopaminergic neurons (DAT-Cre) were asymptomatic. Adult-onset conditional deletions of Kcna1 also produced only mild sleep loss 6 weeks later. To survey the molecular landscape in Kcna1-/- mice, we conducted a mass spectrometry proteomic analysis of dissected hippocampal tissue (a predominant seizure onset zone and where astrogliosis is observed). This revealed significant upregulations in brain-derived neurotrophic factor (BDNF) and the immediate early transcription factor, early growth response-3 (EGR3), which is necessary for the induction of BDNF following electroconvulsive seizures. Heterozygous or homozygous deletions of Egr3 in Kcna1-/- mice resulted in significant survival prolongation, a partial suppression of neurobehavioral impairments, and a significant reduction in the frequency of spontaneous seizures and spreading depolarization events. These phenotypic corrections were associated with an amelioration of BDNF induction, hippocampal astrogliosis and proteomic disturbances. Together, these data demonstrate how disruptions to an ion channel that governs neuronal excitability at millisecond timescales can pleiotropically alter spontaneous behavior over much longer time scales. Our results provide a model and a set of precision endpoints to understand how ictal and interictal features of DEE may manifest through long-term transcriptional alterations imparted by early life seizures. - Source: PubMed
Publication date: 2026/09/17
Mazumder Arindam GhoshKaredia SaifinaAdhyapak NandaniSchirmer CatharinaBass John SamuelKamen Jessica LJankovic Miranda JMiao QinglongGallitano Amelia LSaltzman Alexander BJain AntrixMalovannaya AnnaGlasscock EdwardAiba IsamuNoebels Jeffrey LKrishnan Vaishnav - How cell-type-specific nucleus accumbens (NAc) circuits encode social interactions, and whether this encoding is disrupted in autism spectrum disorder (ASD), remains unresolved. Using longitudinal miniscope calcium imaging and optogenetics in mice, we show that NAc core population activity selectively encodes social interaction and that NAc inhibition enhances sociability. In Cntnap2 mice, both acute and cross-day social representations are degraded, and NAc inhibition persistently improves sociability. Cell-type-specific recordings and optogenetics reveal opposing medium spiny neuron (MSN) contributions: D1-MSNs promote sociability, and D2-MSNs suppress it. Cntnap2 mice exhibit selective depletion of socially excited D1-MSNs and socially inhibited D2-MSNs, along with impaired cross-day population decoding. D2-MSN inhibition improves social behavior in Cntnap2 mice, and D1-MSN activation does not. Together, these findings link disrupted, cell-type-specific NAc social representations to ASD-related social dysfunction and suggest that targeted modulation of NAc activity may improve social behavior. - Source: PubMed
Publication date: 2026/09/10
Zhao PingpingChen XingBellafard ArashMurugesan AvaneeshQuan JonathanAharoni DanielGolshani Peyman - - Source: PubMed
Sun JZhou Y WCheng CHe X YLu J ZQian X YLi AGao X - Autoimmune encephalitis (AE) is a heterogeneous group of immune-mediated disorders of the central nervous system characterized by neuropsychiatric symptoms, seizures, cognitive decline, and movement abnormalities. Timely recognition and initiation of immunotherapy are critical to improving outcomes. We report three cases of AE presenting with varied clinical phenotypes from the Neurology department of Madras Medical College. The first, a 44-year-old male, presented with altered sensorium, action tremor, and myokymia, and was diagnosed with LGI1 and CASPR2 antibody-positive AE. The second, a 16-year-old girl, presented with seizures, progressive cognitive decline, behavioral disturbance, and focal weakness, confirmed as anti-NMDAR encephalitis. The third, a 14-year-old boy, developed seizures and behavioral changes following herpes simplex encephalitis and was later confirmed to have anti-NMDAR antibody-positive AE with features of Kluver-Bucy syndrome. All patients received first-line immunotherapy (steroids, IVIg), with escalation to rituximab in resistant cases. - Source: PubMed
Publication date: 2026/09/04
Kumar N S ManojKumar A SanthoshAnbalagan VigneshVijay Marian JudeSundaram N ShanmugaKrishnan Mugundhan - Autism spectrum disorder (ASD) is a clinically and genetically heterogeneous neurodevelopmental condition. Whole‑exome sequencing (WES) is a pivotal diagnostic tool, though its yield varies across populations. This study aimed to determine the diagnostic yield and characterize the genetic spectrum identified by WES in a pediatric ASD cohort from Saudi Arabia. - Source: PubMed
Publication date: 2026/08/17
Alasiri AbdulazizAl-Jabri BasmahAbukhaled MusaedAldhalan HeshamAl Eman NoorAlmogren SaraAlodah NoraAlhamoudi SaadAlyazidi Anas