SEMA3A (P737) pAb host: Rabbit
- Known as:
- SEMA3A (P737) pAb production species: Rabbit
- Catalog number:
- bs3691
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Bioworld
- Gene target:
- SEMA3A (P737) pAb host: Rabbit
Related genes to: SEMA3A (P737) pAb host: Rabbit
- Gene:
- PPP1R18 NIH gene
- Name:
- protein phosphatase 1 regulatory subunit 18
- Previous symbol:
- KIAA1949
- Synonyms:
- phostensin
- Chromosome:
- 6p21.33
- Locus Type:
- gene with protein product
- Date approved:
- 2004-03-02
- Date modifiied:
- 2016-10-05
- Gene:
- SEMA3A NIH gene
- Name:
- semaphorin 3A
- Previous symbol:
- SEMAD
- Synonyms:
- SEMA1, SemD, coll-1, Hsema-I
- Chromosome:
- 7q21.11
- Locus Type:
- gene with protein product
- Date approved:
- 1999-06-25
- Date modifiied:
- 2016-10-05
Related products to: SEMA3A (P737) pAb host: Rabbit
guanine nucleotide binding protein alpha inhibiting activity polypeptide 1 (GNAI1) polyclonal antibody kinase suppressor of ras (KSR) polyclonal antibody'F 4_80 Antigen (mouse) Host Rat'F 4_80 Antigen (mouse) Host Rat(Alpha)_ 1 _ antitrypsin (A1AT) POLYCLONAL Rabbit anti_human(Alpha)_ Feto Protein (AFP) POLYCLONAL Rabbit anti_human(Alpha)_ Feto Protein (AFP) POLYCLONAL Rabbit anti_human(Alpha)_1_ antitrypsin (A1AT) POLYCLONAL Rabbit anti_human(Arg6,b_cyclohexyl_Ala8,D_Tic16,Arg17,Cys18)_Atrial Natriuretic Factor (6_18) amide (mouse, rabbit, rat) Salt _ Binding (Disulfide_bond) Synonym A71915 SumFormula C69H116N26O15S2(Arg6,b_cyclohexyl_Ala8,D_Tic16,Arg17,Cys18)_Atrial Natriuretic Factor (6_18) amide (mouse, rabbit, rat) Salt _ Binding (Disulfide_bond) Synonym A71915 SumFormula C69H116N26O15S2(Arg6,β-cyclohexyl-Ala8,D-Tic16,Arg17,Cys18)-Atrial Natriuretic Factor (6-18) amide (mouse, rabbit, rat)
A71915 98% C69H116N26O15S2 CAS:(Arg8)-Vasopressin - Diluted Antiserum for RIA, Host Guinea Pig(Arg8)-Vasopressin - Diluted Antiserum for RIA, Host Rabbit(Arg8)-Vasopressin - Diluted Antiserum for RIA, Host: Guinea Pig(Arg8)-Vasopressin - Diluted Antiserum for RIA, Host: Guinea Pig Related articles to: SEMA3A (P737) pAb host: Rabbit
- Chronic stress-induced osteoporosis is a prevalent yet therapeutically challenging condition, with sympathetic overactivation as a key contributor. The dominant pathological mediator and strategies for its precise, non-invasive modulation remain unclear. Here, we identify sympathetic neuropeptide Y as a critical driver of this pathology. Using an unpredictable chronic mild stress model in male mice, we show that neuropeptide Y directly induces cellular senescence in bone marrow adipocytes, thereby impairing osteogenesis. Pulsed electromagnetic field treatment rescued bone loss in wild-type mice, but not in mice with sympathetic neuron-specific deletion of neuropeptide Y (Th;NPY), demonstrating that neuropeptide Y suppression is required for pulsed electromagnetic field efficacy. Mechanistically, pulsed electromagnetic field action depends on intact sensory innervation and operates through the adipocyte neuropeptide Y receptor Y1R. We further delineate a novel peripheral circuit: pulsed electromagnetic field activates sensory nerves to trigger local release of semaphorin 3 A, which in turn directly suppresses sympathetic neuropeptide Y secretion within the bone marrow microenvironment-a mechanism validated by in vitro co-culture and semaphorin 3 A blockade. This sensory-sympathetic feedback loop functions autonomously, independent of central pathways. Our study reveals a local interoceptive mechanism by which pulsed electromagnetic field counteracts stress-induced osteoporosis, positioning peripheral neuropeptide Y -Y1R signaling as a precise target for neuromodulatory therapy. - Source: PubMed
Publication date: 2026/09/29
Wang TiantianLiang ZejunZeng WenjuanChen JiehaoWang ChangyiGong XueChen SihanZhou YaojiaWu HongbinTang LinqiaoMa YaruZhou DongHong Zhen - After traumatic injury to the central nervous system (CNS), meningeal fibroblasts migrate into the lesion site and synthesize extracellular matrix (ECM) molecules, leading to the formation of a fibrotic scar (FS). The FS prevents axonal regeneration by releasing inhibitory ECMs, including chondroitin sulfate proteoglycans, Slits, and semaphorin 3A. Platelet-derived growth factor (PDGF) has been implicated in fibrotic diseases, but its specific contribution to FS formation has remained unclear. In this study, we investigated the role of PDGF signaling in scar formation after CNS injury. In the lesioned mouse brain, PDGFRα and PDGFRβ were strongly expressed within the FS, while PDGF-B was detected in reactive astrocytes surrounding the lesion. Administration of AG1296, a PDGF signaling inhibitor, into the lesion site significantly reduced FS formation and allowed partial regeneration of transected dopaminergic axons. Complementary in vitro studies using rat meningeal fibroblasts demonstrated that PDGF signaling promoted both proliferation and migration of fibroblasts. Moreover, PDGF stimulation enhanced expression of transforming growth factor-β (TGF-β), a cytokine known to drive ECM deposition and scar formation. These findings provide the first direct evidence that inhibition of PDGF signaling suppresses FS formation and facilitates axonal regeneration after CNS lesioning. Our results suggest that PDGF signaling functions during the early phase of FS development by promoting fibroblast proliferation, migration, and TGF-β expression. Thus, targeting PDGF signaling may represent a promising therapeutic strategy for limiting scar formation and improving neural repair following human CNS injury. - Source: PubMed
Publication date: 2026/09/29
Komuta YukariKimura-Kuroda JunkoSeko YukoHongo YuSuzuki KazushiKawano Hitoshi - - Source: PubMed
Publication date: 2026/09/19
Rezaeepoor MahsaShapoori ShimaGanjalikhani-Hakemi MazdakEtemadifar MasoudAlsahebfosoul FereshtehEskandari NahidMansourian Marjan - Multiple myeloma (MM) is a malignant plasma cell disease inducing osteolytic lesions by disrupting bone homeostasis, fostering catabolic and suppressing anabolic functions. While the impact on osteoblast generation and function is well documented, alterations of osteocyte function and extracellular matrix (ECM) are not yet fully understood. Thus, using a syngeneic mouse model of MM by injecting MOPC315.BM cells intratibially into BALB/c mice (n = 95), we performed transcriptomic profiling of an osteocyte-enriched population and identified a mechanosensitive matrisomal gene signature, which was disrupted by tumor engraftment. Non-invasive tibial loading restored the expression of 94 ECM-associated genes, including collagens, fibronectin, and aggrecan. Cross-species integration with RNA-sequencing data from 387 MM patients revealed eight ECM-related genes whose expression correlated with overall survival (VEGFA, BCAN, FGF13, TNFSF8, SDC1, LAMC1, SEMA3A, and CCL2). Four of these genes (Vegfa, Sdc1, Sema3a, Ccl2) were also load-responsive in a murine osteocyte (IDG-SW3 cells) bioreactor model. Our findings indicate that an existing mechanosensitive osteocytic repair program is suppressed by MM cells, which can be reinvigorated via a brief single loading session. It suggests that exercise-based interventions may be beneficial to restore bone mass through endochondral ossification programs in patients with MM. - Source: PubMed
Publication date: 2026/09/07
Ziouti FaniAzeem MuhammadRummler MaximilianRosolowski MaciejZapata GerardoRindt WyonnaJulien CatherineTauer Josephine TCheng Wen-HuiBeck SusanneSeckinger AnjaHose DirkLeich EllenBogen BjarneLynch Maureen EKuric MartinKrug MelanieEbert ReginaZaucke FrankJakob FranzWillie Bettina MJundt Franziska - Peri-implantitis, a major cause of implant failure, is driven by disrupted bone homeostasis. Semaphorin 3A (Sema3A) bidirectionally regulates bone remodelling, yet its role in peri-implantitis remains poorly defined. This study aimed to elucidate the mechanisms by which Sema3A modulates bone homeostasis in peri-implantitis. - Source: PubMed
Publication date: 2026/09/03
He ChenjiangDai FangWu JingtingDeng LibinJiang MeixiuYang YutingLi LiXu FanchengSong Li