PTPRC Antibody
- Known as:
- PTPRC Antibody
- Catalog number:
- XW-7814
- Product Quantity:
- 0.05 mg
- Category:
- -
- Supplier:
- Prosci
- Gene target:
- PTPRC Antibody
Related genes to: PTPRC Antibody
- Gene:
- PTPRC NIH gene
- Name:
- protein tyrosine phosphatase receptor type C
- Previous symbol:
- CD45
- Synonyms:
- LCA, T200, GP180
- Chromosome:
- 1q31.3-q32.1
- Locus Type:
- gene with protein product
- Date approved:
- 1986-01-01
- Date modifiied:
- 2019-04-23
Related products to: PTPRC Antibody
Related articles to: PTPRC Antibody
- Dental pulp stem cells (DPSCs), a subset of mesenchymal stem/progenitor cells, exhibit remarkable self-renewal and multipotent differentiation capacity, making them promising candidates for regenerative applications. While their in vitro characteristics have been extensively studied, the in vivo dynamics and molecular regulation during development are much less known. This study examined the embryonic/prenatal (E16.5) and early postnatal (P3.5 and P7.5) stages of mouse molar development to trace the temporospatial expression and overlap of five key molecules associated with DPSC: a trio of positive markers (CD73/Nt5e, CD90/Thy1, and CD105/Eng) and two negative markers (CD34/Cd34 and CD45/Ptprc). Reanalysis of single-cell RNA sequencing data revealed a triple-positive and double-negative population overlapping in the dental mesenchyme by P7.5. The results were confirmed by multiple immunofluorescence-based in situ labeling. These findings contribute to the understanding of the spatiotemporal in vivo expression landscape and dynamics of DPSC markers, thus bridging the gap between in vitro characterization and the complex developmental reality of the dental pulp. - Source: PubMed
Publication date: 2026/09/24
Holomková KateřinaYamada ShuntaroŠvandová EvaMatalová EvaHovhannisyan Jesica HasmikKrikorian TaleenBagdasarian LidiiaAyvazyan SonaAzadians DinoLesot HervéJanečková Eva - Cancer-associated fibroblasts (CAFs) are key components of the melanoma tumor microenvironment and have been implicated in immune evasion and therapy resistance. However, the spatial relationships between CAFs, extracellular matrix (ECM) remodeling, and immune exclusion remain incompletely characterized. - Source: PubMed
Publication date: 2026/09/15
Zheng WeilongZheng Huanhuan - The co-occurrence of liver cirrhosis (LC) and heart failure (HF) poses considerable clinical challenges, yet the cellular and molecular determinants of this comorbidity remain poorly characterized. To address this, we developed an integrative multi-omics pipeline encompassing GWAS meta-analysis, gsMap-based spatial transcriptomic projection, GeneEnrich functional annotation, single-cell atlas construction, seismicGWAS and ECLIPSER cell-type scoring, eCAVIAR and fastenloc colocalization, hdWGCNA network inference, scTenifoldKnk in silico gene perturbation, and GCTA-COJO fine-mapping. Quality-controlled meta-analysis yielded 12,347,758 and 9,256,862 variant-level associations for LC and HF, respectively. Spatial projection confirmed preferential enrichment of disease signals within embryonic hepatic and cardiac compartments. Pathway analyses disclosed that LC-linked loci were concentrated in lipid metabolic programs, whereas HF-linked loci implicated mitochondrial bioenergetics and lysosomal degradation. At the cellular level, endothelial cells emerged as the dominant HF-associated population. Convergent evidence from five orthogonal algorithms pinpointed CRIM1 as the sole robustly supported shared gene, selectively enriched in HF endothelial cells; virtual perturbation further identified LCP1 and PTPRC as downstream regulatory nodes. Fine-mapping of the chromosome 2 locus harboring rs12476437 revealed multiple statistically independent signals in the vicinity of CRIM1. Collectively, these findings computationally prioritize the endothelial-CRIM1 axis as a previously unappreciated candidate mechanistic bridge between LC and HF requiring experimental validation. - Source: PubMed
Publication date: 2026/09/06
Zhao RuiqiGuo JieshengHan MengyaoTang ShiqiHu HuiMa MengqingSun JialingZhou Xiaozhou - Among the more than 90 identified genetic risk loci for late-onset Alzheimer's disease (AD) and related dementias, the apolipoprotein E (APOE) gene ɛ2/ɛ3/ɛ4 polymorphisms remain the longstanding benchmark for genetic disease risk with a consistently large effect across studies. Despite this massive signal, the exact mechanisms by which ɛ4 increases and ɛ2 decreases dementia risk remain poorly understood. Notably, recent trials of anti-amyloid therapies suggest less efficacy and higher risks of severe side effects in ε4 carriers, hampering the treatment of those with the highest unmet need. To improve our understanding of the genetic architecture of AD in the context of its main genetic driver, we performed genome-wide association studies (GWASs) stratified by ε4 and ε2 carrier status. HP1BP3, SLC50A1, PTPRC, NPAS3, DDHD1, CHST9, SMYD2, PRAMEF1 and GFRA1 emerged as new genomic signals for AD risk, appearing only when stratified by APOE carrier status. DDHD1 appeared especially promising, showing protective effects in ε4 carriers, being identified as an expression quantitative trait locus and being involved in rare neuronal diseases. Such APOE-stratified insights may help understand and overcome side effects, inform clinical trial enrollment strategies, and create the scientific basis for targeted, mechanism-driven therapies in neurodegenerative diseases. - Source: PubMed
Publication date: 2026/09/14
Thomassen Jesper QvistLeonard HamptonUlms BrittanyGrenier-Boley BenjaminHeikkinen SamiGarcia-González PabloCastillo-Morales AtahualapaKikuchi MasatakaGim JungsooCao HanKüçükali FahriAmin NajafYoon Dabinde Rojas ItziarAlvarez Jerez PilarAlvarez VictoriaArosio BeatriceBellenguez CélineBergh SverreBillingsley KimberleyBlauwendraat CornelisBoada MerceBorroni BarbaraBossù PaolaBullido María JDaniele AntonioCarracedo Ángelde Mendonça AlexandreCookson MarkDeckert JürgenDichgans MartinDjurovic SrdjanDols-Icardo OriolDufouil CaroleDüzel EmrahEscott-Price ValentinaFladby TormodFratiglioni LauraFu Amy K YGalimberti DanielaGarcía-Alberca Jose MariaGiedraitis VilmantasGarcia-Ribas GuillermoGraff CarolineGrimmer TimoGrünblatt EdnaHanon OlivierHausner LucreziaHeilmann-Heimbach StefanieHort JakubJessen FrankJensen KendallJonson CarolineKim YoontaeKuznetsov NicoleLeinonen VilleLipponen AnssiLuo JiaoMakarious MaryMartiskainen HennaMasullo CarloMecocci PatriziaMehrabian ShimaMir PabloMiyashita AkinoriMoebus SusanneMok Kin YMolina Porcel LauraMoreno FerminNacmias BenedettaParnetti LucillaPastor PauPérez-Tur JordiPeters OliverPijnenburg Yolande A LPiñol-Ripoll GerardPopp JuliusRainero InnocenzoReal Luis MRiedel-Heller SteffiRodriguez-Rodriguez EloyRongve ArvidRossi GiacominaRoyo Jose LuisRujescu DanSaltvedt IngvildSáez María EugeniaSánchez-Valle RaquelSanchez-Garcia FlorentinoSandau NicolaiScarmeas NikolaosScheffler KatjaScherbaum NorbertSchneider AnjaSelbæk GeirSeripa DavideSolfrizzi VincenzoSpallazzi MarcoSquassina AlessioStordal EysteinTesi NiccolóTremolizzo LucioTripathi Kumar Pvan der Flier Wiesje MWilliams JulieWiltfang JensAarsland DagSingleton Andrew BAmouyel PhilippeDebette StéphanieTsolaki MagdaNicolas Gaelvan der Lee SvenHolstege HenneFernandez Maria VictoriaKehoe Patrick GavinSleegers KristelIngelsson MartinGhidoni RobertaAndreassen Ole AHolmans Peter ASánchez-Juan PascualSims RebeccaIp Nancy YLee Kun HoIkeuchi TakeshiRamirez AlfredoRuiz AgustinHiltunen MikkoLambert Jean-Charlesvan Duijn CorneliaNalls MikeFrikke-Schmidt Ruth - [This corrects the article DOI: 10.3389/fimmu.2024.1446931.]. - Source: PubMed
Publication date: 2026/08/12
Michalik JurajNiederlova VeronikaStepanek Ondrej