Human SEMA4D _CD100 Protein Vector: HEK293
- Known as:
- Human SEMA4D _CD100 Protein Vector: HEK293
- Catalog number:
- 10098-H03H
- Product Quantity:
- 100μg
- Category:
- -
- Supplier:
- Provo
- Gene target:
- Human SEMA4D _CD100 Protein Vector: HEK293
Related genes to: Human SEMA4D _CD100 Protein Vector: HEK293
- Gene:
- SEMA4D NIH gene
- Name:
- semaphorin 4D
- Previous symbol:
- SEMAJ, C9orf164
- Synonyms:
- CD100, coll-4, FLJ39737
- Chromosome:
- 9q22.2
- Locus Type:
- gene with protein product
- Date approved:
- 1999-06-25
- Date modifiied:
- 2016-10-05
Related products to: Human SEMA4D _CD100 Protein Vector: HEK293
Related articles to: Human SEMA4D _CD100 Protein Vector: HEK293
- Inhibitory synapse formation is poorly understood compared to excitatory synaptogenesis, in part because the molecular events underlying assembly occur asynchronously and on timescales that have been difficult to resolve. Here, we exploit the ability of Semaphorin 4D (Sema4D) to rapidly and selectively induce GABAergic synapse formation in cultured hippocampal neurons, synchronizing these events to enable direct observation of pre- and postsynaptic protein dynamics by two-channel live imaging. We find that Sema4D promotes a population-wide increase in the mobility of GAD65-containing presynaptic boutons within 20 minutes of treatment while postsynaptic gephyrin scaffolds are mobilized only locally in a proximity-dependent manner, consistent with a presynapse-first model of inhibitory synapse assembly. Sema4D also drives recruitment of GABARγ2 subunits to receptor-poor postsynaptic gephyrin scaffolds within 10 minutes of treatment, prior to detectable changes in GAD65-gephyrin colocalization, suggesting that postsynaptic scaffolds are primed for receptor capture before alignment with a presynaptic partner. Finally, we observe new colocalization events between established gephyrin and GABAR protein assemblies, suggesting that clustering of either the gephyrin scaffold or GABARs alone is sufficient to nucleate assembly of the postsynaptic specialization. Together, these results reveal a temporally ordered, spatially constrained mechanism by which Sema4D coordinates pre- and postsynaptic protein dynamics to assemble inhibitory synapses on the timescale of minutes. The assembly of new synaptic contacts requires precise coordination of specialized proteins in pre- and postsynaptic neurons. Inhibitory synapses, which suppress neuronal activity and are essential for circuit stability, contain distinct molecular components, yet the mechanisms governing their assembly remain poorly understood. We used Sema4D, a protein that rapidly induces inhibitory synapse formation, as a molecular tool to dissect how synaptic proteins on either side of the synaptic cleft are coordinated in space and time. Using live imaging we show that Sema4D acts on both pre- and postsynaptic compartments to recruit synaptic proteins with spatiotemporal precision. Together, these findings define the sequence of molecular events underlying inhibitory synapse assembly and have implications for neurodevelopmental disorders in which inhibition is disrupted. - Source: PubMed
Publication date: 2026/05/19
Pranske ZacharyParadis Suzanne - Semaphorin 4D (Sema4D)/(CD100) expression is upregulated in different human cancers, and it is associated with poor prognosis; however, its prognostic value in B-acute lymphoblastic leukemia (B-ALL) remains unclear. We aimed to study the prognostic value of Sema4D expression to predict response to induction therapy in pediatric patients with B-ALL. Sixty newly diagnosed pediatric patients with B-ALL were enrolled, and their peripheral mononuclear cells (PBMCs) were isolated for assessment of Sema4D expression by multiparametric flow cytometry before initiating therapy. Then, we followed up with the patients for their response to induction therapy. Sema4D expression is significantly higher in non-responders to induction therapy than in responders. Using the receiver operating characteristic (ROC) curve, Sema4D expression > 18% significantly identifies patients at risk for induction failure. Logistic regression analyses confirmed that Sema4D expression is significantly associated with poor response to induction therapy. - Source: PubMed
Publication date: 2026/04/17
Elkholy Rasha AEl Amrousy DoaaElgezawy Doaa EElkholy Reem ATaha OlaEltoukhy Abeer AElaskary Eman - Single-cell fixed RNA profiling (FLEX) is a novel technique that captures RNA expression in frozen tissues at a single-cell resolution. We applied FLEX to mouse model of liver fibrosis progression and regression to identify novel antifibrotic targets. - Source: PubMed
Publication date: 2026/02/11
Duc Pham MinhThuy Le Thi ThanhHai HoangVan Bao TranHa Nguyen ThiAnh Pham TuanIkenaga HirokoFujii HidekiYoshida KanakoEnomoto MasaruUchida-Kobayashi SawakoYuasa HidetoMatsubara TsutomuHuyen Vu ThuongCheng YiYamagishi RyotaOhtani NaokoOikawa DaisukeTokunaga FuminoriKisseleva TatianaBrenner David AIwakiri YasukoGracia-Sancho JordiKawada Norifumi - Psoriasis is an autoimmune systemic disease of not entirely understood pathogenesis. It remains a significant therapeutic challenge and, due to its various comorbidities, has a remarkable detrimental effect on patients' wellbeing. Semaphorins (Sema) are a group of transmembrane, cell surface-attached and secretory proteins that might play an important role in psoriasis due to their presence on keratinocytes and the ability to stimulate the proinflammatory cytokine production. - Source: PubMed
Publication date: 2026/03/12
Baran AnnaStepaniuk AnnaHermanowicz Justyna MagdalenaSieklucka BeataPawlak KrystynaPawlak DariuszFlisiak Iwona - Periodontitis is a chronic inflammatory disease that severely affects oral and general health. N7-methylguanosine (m7G) methylation plays critical roles in regulating gene expression and cellular functions. Methyltransferase-like 1 (METTL1), a core component of the m7G methyltransferase complex, has been implicated in various diseases, but its role in periodontitis remains unclear. - Source: PubMed
Publication date: 2026/03/13
Huang Yong-SongZhang Zi-HaoZhou Mei-YunGeng Lin-YaWang Ting-Ting