NRP1 _ Neuropilin_1 Protein
- Known as:
- NRP1 _ Neuropilin_1 Protein
- Catalog number:
- 10011-H02H
- Product Quantity:
- 50
- Category:
- -
- Supplier:
- Smart Serology
- Gene target:
- NRP1 _ Neuropilin_1 Protein
Related genes to: NRP1 _ Neuropilin_1 Protein
- Gene:
- NRP1 NIH gene
- Name:
- neuropilin 1
- Previous symbol:
- -
- Synonyms:
- NRP, VEGF165R, CD304
- Chromosome:
- 10p11.22
- Locus Type:
- gene with protein product
- Date approved:
- 1998-12-23
- Date modifiied:
- 2016-10-05
Related products to: NRP1 _ Neuropilin_1 Protein
Related articles to: NRP1 _ Neuropilin_1 Protein
- Pathogen-host interaction plays key roles in the pathogenesis of infectious diseases. The miR-183/96/182 cluster (miR-183C) is highly expressed in trigeminal ganglion (TG) sensory neurons (SNs) and modulates corneal response to (PA) infection. To uncover the molecular mechanisms of miR-183C modulating the interactions of PA and TG SN, we employed the miR-183C conventional knockout (KO) or sensory neuron-specific (SNS) conditional (C)KO mouse models. Trigeminal ganglion (TG) SNs were isolated for neurite growth and branching analyses. Neuropeptide and chemokine production by TG SNs in response to PA infection was studied by ELISA assays. Key target genes of miR-183C were validated by target luciferase reporter assays. Our data showed that the total neurite length and number of branches per TG SN were decreased in the CKO vs. WT mice, and in the male vs. female WT mice. PA infection of TG SN induced the production and secretion of CX3CL1 and substance P (sP); this response was significantly enhanced in miR-183C KO vs. WT mice. Antagonists to Toll-like receptor (TLR)4 and/or formyl peptide receptor (FPR)1 inhibited PA-induced responses. Target luciferase reporter assays confirmed that genes encoding TLR4 and FPR1, as well as NRP1-a repulsive axon guidance receptor, TAC1-the precursor gene of sP, CX3CL1 and ADAM10, a metalloproteinase involved in the production of soluble CX3CL1, were direct targets of miR-183C. These data suggest that PA directly activates TG SNs and induces chemokine and neuropeptide production/secretion through interactions with TLR4 and FPR1. miR-183C modulates this process by targeting a collection of key genes involved in axon guidance/projection, chemokine and neuropeptide biogenesis and receptors mediating PA-induced activation. - Source: PubMed
Publication date: 2026/08/03
LoGrasso GiovanniGupta NamanBugulu Sai Giridhar ReddyHazlett Linda DLeger Anthony J StXu Shunbin - Propensity score-matched comparison of 23 SGLT2 inhibitor users and 23 non-users revealed that SGLT2 inhibitor use was associated with significantly lower Neuropilin-1 (NRP1) levels (74.25 vs. 87.61 ng/mL; p = 0.015) and a higher Sema3A/NRP1 ratio (0.14 vs. 0.12; p = 0.006), indicating functional impairment of the Sema3A/NRP1/Plexin-A1 bone signaling axis with compensatory Sema3A upregulation. Classical bone turnover markers (P1NP, CTX, coupling index) and DXA-derived BMD did not significantly differ between groups. These findings suggest that SGLT2 inhibitors may perturb the Sema3A/NRP1/Plexin-A1 axis before detectable changes in conventional markers, offering a novel mechanistic perspective to explain the inconsistency between existing meta-analyses on SGLT2 inhibitor bone safety. - Source: PubMed
Erarslan SertasBora Burcu Cosgun - Transcription factor homeobox C9 (HOXC9) has been reported to be up-regulated and associated with poor prognosis in colorectal cancer (CRC). This study focused on the regulatory role and molecular mechanism of HOXC9 in CRC progression and immune response. Differential analysis from the GSE25070 dataset was performed. The mRNA and protein levels of target genes were measured using qPCR and Western blotting. Malignant behaviors in LoVo and Caco2 cells were assessed using colony formation assay, transwell assay and tumor sphere formation assay. Programmed death ligand 1 (PD-L1) expression on cell surface was detected using flow cytometry. LoVo and Caco2 cells were co-cultured with CD8 + T cells, followed by apoptosis detection using flow cytometry and quantification of immune-related mRNA using qPCR. Role of HOXC9 in vivo was explored through xenograft tumor assay. Interaction between HOXC9 and neuropilin 1 (NRP1) was validated via chromatin immunoprecipitation (ChIP) and dual-luciferase reporter assay. HOXC9 was upregulated and predicted a poor prognosis in CRC. Silencing HOXC9 suppressed CRC cell proliferation, migration, invasion, cell stemness, down-regulated PD-L1 expression and promoted anti-tumor immune function of CD8 + T cells. HOXC9 knockdown reduced CRC tumor growth and PD-L1 expression in vivo. HOXC9 elevated NRP1 expression via transcriptional activation of NRP1. NRP1 overexpression could reverse CRC progression inhibition and immune function enhancement caused by HOXC9 downregulation. These findings elucidate a specific mechanism whereby HOXC9 transcriptionally activates NRP1, thereby contributing to CRC malignant development and immune evasion. - Source: PubMed
Publication date: 2026/08/25
Qiu XiaofengHu ShengLiao BinglingZhang HuijunTang YunchengXu Qihua - Proper neocortex formation relies on the precisely regulated migration of neurons into distinct cortical layers. This process requires the timely surface expression of receptors that decode extracellular guidance cues. Yet, the molecular machinery governing receptor trafficking in migrating neurons remains largely unclear. Here, we identified the motor protein myosin Va (Myo5a) as a key regulator of Neuropilin-1 (Nrp1) trafficking in the early postnatal neocortex. Both male and female mice were used for this study. Myo5a localized to the apical dendrites of superficial layer neurons, with expression increasing during cortical maturation. Functional inhibition of Myo5a led to a terminal translocation defect in superficial layer neurons, thereby preventing their proper entry into NeuN-negative regions of the neocortex. Additionally, Myo5a inhibition led to Nrp1 accumulation within the Golgi apparatus and a significant reduction in its surface expression. Remarkably, overexpression of Nrp1 or VLDLR fully rescued the terminal translocation defects and dendritic abnormalities caused by Myo5a inhibition, demonstrating that Myo5a-dependent Nrp1 trafficking underlies proper Reelin receptor availability during this process. Overall, these results reveal a pivotal Myo5a-Nrp1 trafficking pathway that governs the final stage of neuronal migration, offering a molecular mechanism for the spatial and temporal regulation of receptor dynamics essential for precise cortical layering. Proper neocortex formation is essential for establishing functional brain circuits; however, the mechanisms by which migrating neurons interpret extracellular cues remain poorly understood. This study identified the motor protein Myo5a as a key regulator of the cell-surface expression of the Reelin coreceptor Nrp1 during the final phase of neuronal migration. Myo5a inhibition disrupts Nrp1 trafficking to the plasma membrane , leading to terminal translocation defects and abnormal dendritic development. Overexpression of Nrp1 or VLDLR fully rescues both phenotypes, indicating that Myo5a-dependent Nrp1 trafficking is essential for proper Reelin receptor availability at the cell surface. These findings reveal a previously unrecognized mechanism that enables neurons to respond properly to Reelin signaling, thus ensuring precise cortical layer formation during brain development. - Source: PubMed
Publication date: 2026/08/24
Kohno TakaoOkino RimiLi MinqianHattori Mitsuharu - Glioblastoma (GBM) is the most aggressive and malignant primary brain tumor in adults, characterized by rapid growth, diffuse invasion, marked intratumoral heterogeneity, and resistance to conventional therapies. Semaphorin-Plexin signaling, originally identified as a key regulator of axonal guidance during nervous system development, has subsequently emerged as a critical pathway involved in multiple aspects of cancer biology, including tumor proliferation, invasion, angiogenesis, immune modulation, and therapeutic resistance. - Source: PubMed
Publication date: 2026/08/06
Prajapati ShatrudhanSingh Ajay PalTripathi VashnaviYadav Shikha