CD40L (CD154) mAb;human (5F3)
- Known as:
- CD40L (CD154) mAb;H. sapiens (5F3)
- Catalog number:
- ASACSA-187E
- Product Quantity:
- 100 µg
- Category:
- -
- Supplier:
- Other suppliers
- Gene target:
- CD40L (CD154) mAb;human (5F3)
Related genes to: CD40L (CD154) mAb;human (5F3)
- Gene:
- CD40LG NIH gene
- Name:
- CD40 ligand
- Previous symbol:
- HIGM1, IMD3, TNFSF5
- Synonyms:
- CD40L, TRAP, gp39, hCD40L, CD154
- Chromosome:
- Xq26.3
- Locus Type:
- gene with protein product
- Date approved:
- 1989-06-30
- Date modifiied:
- 2019-04-23
- Gene:
- HERC2 NIH gene
- Name:
- HECT and RLD domain containing E3 ubiquitin protein ligase 2
- Previous symbol:
- -
- Synonyms:
- jdf2, p528, D15F37S1
- Chromosome:
- 15q13.1
- Locus Type:
- gene with protein product
- Date approved:
- 1999-01-07
- Date modifiied:
- 2016-10-05
- Gene:
- HERC2P1 NIH gene
- Name:
- hect domain and RLD 2 pseudogene 1
- Previous symbol:
- -
- Synonyms:
- D15F37S2
- Chromosome:
- 15q13
- Locus Type:
- pseudogene
- Date approved:
- 1999-01-07
- Date modifiied:
- 2014-11-19
- Gene:
- HERC2P2 NIH gene
- Name:
- hect domain and RLD 2 pseudogene 2
- Previous symbol:
- -
- Synonyms:
- D15F37S3
- Chromosome:
- 15q11.2
- Locus Type:
- pseudogene
- Date approved:
- 1999-01-07
- Date modifiied:
- 2015-02-02
- Gene:
- HERC2P3 NIH gene
- Name:
- hect domain and RLD 2 pseudogene 3
- Previous symbol:
- -
- Synonyms:
- D15F37S4, LOC283755
- Chromosome:
- 15q11.1-q11.2
- Locus Type:
- pseudogene
- Date approved:
- 1999-01-07
- Date modifiied:
- 2018-02-13
Related products to: CD40L (CD154) mAb;human (5F3)
Related articles to: CD40L (CD154) mAb;human (5F3)
- Hospitalization in older adults often leads to disability in daily living activities, thereby increasing the risk of functional and cognitive impairments. This randomized controlled trial analyzed the serum protein profile of patients admitted to an acute geriatric unit who engaged in supervised multicomponent functional exercises compared with a control group. Potential protein biomarkers were assessed using Olink® serum proteomics platform employing two predefined panels: Cardiometabolic and Inflammation. Notably, short-term exercise intervention was associated with moderate but consistent changes in the serum proteome. Nominal differences (p < 0.05, unadjusted) were observed for amyloid beta precursor-like protein 1 (APLP1), complement C1q tumor necrosis factor-related protein 1 (C1QTNF1), interleukin-8 (CXCL8), interleukin-7 (IL-7), M-phase phosphoprotein 8 (MPHOSPH8), neurotrophin 3 (NTF3), tissue-type plasminogen activator (PLAT), SFRS1-interacting protein (PSIP1), pleiotrophin (PTN), cardiac-type troponin I (TNNI3), von Willebrand factor (vWF), and while levels of CD40 ligand (CD40LG) were reduced. These findings suggest that short-term multicomponent functional exercises during acute hospitalization can induce changes in the serum proteome. These molecular alterations provide exploratory insight into the biological processes associated with the functional benefits observed following the intervention in hospitalized older adult patients. - Source: PubMed
Publication date: 2026/04/30
Izco-Cubero MaiteLachén-Montes MercedesChenhuichen ChenhuiVeloz Ba CedeñoEcheverría-Beistegui IcíarZambom-Ferraresi FabricioZambom-Ferraresi Fabiolade la Riva María Luisa Fernández-GonzálezÁlvarez-Rodríguez PatriciaSantamaría EnriqueMartínez-Velilla Nicolás - Neuroimmune signaling across the peripheral-vascular-glial axis is increasingly recognized as a driver of both age‑related brain vulnerability and the earliest stages of neurodegenerative disease, including Alzheimer disease. Evaluating this axis in vivo remains challenging due to limited neuroinflammatory imaging biomarkers. We utilized [11C]CS1P1 positron emission tomography (PET) to quantify sphingosine-1-phosphate receptor 1 (S1PR1) availability alongside plasma proteomics in 42 cognitively normal individuals (age 21-82). Through differential abundance analysis and structural equation modeling (SEM), we identified a multi-compartment neuroimmune cascade linking peripheral T-cell activation (CD40LG), vascular endothelial disruption (ICAM1/TEK), central S1PR1 upregulation, and reactive astrogliosis (GFAP). Mediation analysis estimated this S1PR1 axis accounts for 25.5% of the total effect of CD40LG on GFAP. This cascade appears coupled to the astrocytic immune response and is exacerbated by underlying amyloid-beta pathology. These findings suggest [11C]CS1P1 may serve as an in vivo tool for evaluating peripheral-to-central immune crosstalk. - Source: PubMed
Publication date: 2026/04/19
Benzinger TammiePowles Savannah TiemannHoagey DavidFlores ShaneyFriedrichsen KarlWu ShuangRajamanickam JayashreeJoseph-Mathurin NellyKeefe SarahNagy SydneyMcKay NicoleWisch JulieSabaredzovic EditaChen GengshengSimmons AshleeJones LynneSoda Anil KumarPowles JonathanDoering StephanieJana NayidMassoumzadeh ParinazBaker BryceCruchaga CarlosSchindler SuzanneIbanez LauraMorris JohnAn HongyuLiu JingxiaTu ZhudeBrier Matthew - Whole blood transfusion is increasingly used in trauma resuscitation. However, stored whole blood units demonstrate increasing susceptibility to tissue plasminogen activator-mediated fibrinolysis despite paradoxical increases seen in plasminogen activator inhibitor-1 (PAI-1) activity over time. Whether early variability in PAI-1activity exists across whole blood units and the biologic contributors to this variability remain unclear. Two distinct donor pools were identified: one with high PAI-1 activity and one with low PAI-1 activity. We set out to determine whether PAI-1 activity in whole blood donors primarily comes from the endothelium or from platelet degranulation. - Source: PubMed
Publication date: 2026/04/23
Maginot Elizabeth RBarmettler Nicolle KGawargi Flobater IMoore Ernest EWhite Collin MHiser Dylan CClegg Ashley ASextro Kyle SMoody Trace BVolk Grace EMoore Hunter BGoodman NatashaBobr AlehHenry ReynoldBarrett Christopher D - The bidirectional interaction between inflammation and thrombus formation plays an important role in myocardial infarction (MI) with IL (interleukin)-6 as a central mediator. If anti-inflammatory therapy modulates coagulation factors, and platelet activation in patients with MI is not clear. - Source: PubMed
Publication date: 2026/04/23
Ueland ThorDahl Tuva BMichelsen AnnikaKleveland OlaAndersen Geir ØysteinAnstensrud Anne KristinHuse CamillaWoxholt SindreBroch KasparGullestad LarsLibby PeterAukrust PålHalvorsen Bente - IL-10-producing B cells exert immunosuppressive effects, yet their low abundance and poor in vitro viability have limited their therapeutic application. Here, we developed a stromal coculture system using MS5 cells engineered to express human CD40L, BAFF, and IFN-β1 (MS5-3F, for "3 factors"), which enables robust induction and greater than 1000-fold expansion of human IL-10-producing B cells. The expanded cells showed phenotypic and transcriptional profiles characteristic of unswitched (IgM+) plasmablasts and potently suppressed CD4+ T cell proliferation in an IL-10-dependent manner. MS5-3F-expanded B cells also increased the frequency of regulatory T cells in vitro, an effect that was not abrogated by IL-10/IL-10R blockade, suggesting contributions from additional mechanisms. IL-10 production originated predominantly from naive B cells, rather than memory B cells. Furthermore, B cells from patients with systemic lupus erythematosus, despite impaired IL-10 production under conventional conditions, were efficiently differentiated into IL-10-producing B cells using this system. The expanded cells showed minimal IgG-secreting output. Our platform offers a scalable strategy for generating human regulatory B cells, laying the foundation for B cell-based immunotherapies. - Source: PubMed
Publication date: 2026/04/22
Kawakami RyoImabayashi KeisukeBaba AkemiSaito YuichiKawata KazuhikoYada YutaroShibata AiriIto RinkaKurasawa RyoHiguchi RyotaPark SungyeonNiiro HiroakiTanaka ShinyaBaba Yoshihiro