CD115 pTyr561 antibody Ab
- Known as:
- CD115 pTyr561 (anti-) Antibody
- Catalog number:
- 1488061
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Acris antibodies
- Gene target:
- CD115 pTyr561 antibody
Related genes to: CD115 pTyr561 antibody Ab
- Gene:
- CSF1R NIH gene
- Name:
- colony stimulating factor 1 receptor
- Previous symbol:
- FMS
- Synonyms:
- C-FMS, CSFR, CD115
- Chromosome:
- 5q32
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-22
- Date modifiied:
- 2015-09-11
Related products to: CD115 pTyr561 antibody Ab
Related articles to: CD115 pTyr561 antibody Ab
- Medulloblastoma is a severe pediatric brain tumor with distinct molecular subtypes-WNT, SHH, Group 3, and Group 4-each having unique genetic drivers and immune microenvironments. This review highlights the immune characteristics of each subtype: SHH is rich in tumor-associated macrophages (TAMs), whose role in tumorigenesis is debated; Group 3 features cytotoxic T cells often neutralized by immune checkpoints like PD-L1, causing T cell exhaustion; and Group 4 is marked by natural killer (NK) cells and B cells. These immune landscapes, including tumor-associated astrocytes (TAAs) and abnormal vascular networks, influence tumor growth, spread, and treatment response. Precision immunotherapy must be tailored to specific subtypes. This article discusses CAR T-cell therapy targeting antigens like B7-H3 and GD2, prevalent in SHH subtypes, and examines immune checkpoint blockades targeting PD-1/PD-L1 and CD47-SIRPα. It also highlights innovative methods like oncolytic viruses to transform "cold" tumor microenvironments and combination therapies using CSF1R inhibitors and tumor-associated antigens to boost anti-tumor responses. Understanding the immune microenvironment's subtype-specific heterogeneity in medulloblastoma is crucial for advancing precision immunotherapy and improving patient outcomes. - Source: PubMed
Publication date: 2026/04/13
Li MengyuanPeng JihongChen ChunHu Jinyang - Epilepsy is one of the most prevalent neurological disorders, affecting over 70 million individuals worldwide. However, despite the introduction of more than 30 anti-seizure medications over three decades, approximately 30% of patients continue to suffer from drug-resistant epilepsy (DRE). Here, we advance the "Senescent Niche Hypothesis," proposing that the epileptogenic focus in DRE harbors a pathological accumulation of senescent microglia that have lost homeostatic surveillance capacity and acquired a toxic secretory phenotype. We present the "Iron-Senescence Axis" as the mechanistic driver: recurrent seizure-induced blood-brain barrier disruption leads to chronic parenchymal iron deposition; microglia accumulate iron through erythrophagocytosis and sustain sub-lethal ferroptotic stress-characterized by lipid peroxidation, mitochondrial dysfunction, and DNA damage-that drives their irreversible transition to a senescent state rather than acute cell death. Once senescent, these microglia paradoxically acquire resistance to ferroptosis through lysosomal iron sequestration, occupy the niche indefinitely, and perpetuate epileptogenesis via the senescence-associated secretory phenotype (SASP), establishing a positive feedback loop. Converging transcriptomic and experimental evidence from both human surgical specimens and rodent models substantiates this framework, demonstrating that senolytic clearance of senescent cells significantly reduces seizure burden and can prevent epilepsy development. Building on these findings, we evaluate two complementary therapeutic strategies: senolytic therapy using dasatinib plus quercetin (D+Q) for selective elimination of senescent cells, and the Microglial Intervention Strategy for Therapy and Enhancement by Replacement (MISTER) for comprehensive niche reconstitution through CSF1R inhibitor-mediated microglial depletion followed by donor cell engraftment. We critically assess donor cell sources, advances in non-genotoxic conditioning, and CSF1R-inhibitor resistant donor cells that may enable clinical translation. This synthesis argues that targeting the senescent microglial niche may represent a disease-modifying approach that shifts the therapeutic focus from seizure suppression to neuroimmune niche restoration. - Source: PubMed
Publication date: 2026/04/10
Wu JinghengLi MiaomiaoShi YetongWang Shuai - Diabetic wounds, particularly diabetic foot ulcers, represent a significant clinical challenge owing to impaired vascularization, persistent inflammation, and dysfunctional extracellular matrix remodeling. Although adipose-derived stem cells offer therapeutic potential, their heterogeneity and functional impairment within the diabetic microenvironment limit their efficacy. Using single-cell RNA sequencing of human adipose and diabetic wound tissues, we identified a distinct CCL2-expressing ADSC subpopulation that is enriched in obese individuals and exhibits elevated stemness, unique metabolic profiles, and enrichment in pathways related to ECM organization and tissue development. This subpopulation functions as a key communication node, engaging with fibroblasts, macrophages, and endothelial cells through ligand-receptor interactions such as CCL2-ACKR1, TGFB1-TGFBR1, and IL34-CSF1R. Exosomes secreted by these CCL2-positive ADSCs were found to be enriched in CCL2, TGFB1, and IL34. In a diabetic mouse wound model, CCL2-ADSC-derived exosomes significantly accelerated wound closure compared with conventional exosomes, promoting angiogenesis, collagen deposition, and M2-macrophage polarization while reducing pro-inflammatory cytokines. In vitro, these exosomes reversed high-glucose-induced suppression of endothelial cell proliferation, migration, and tube formation. Mechanistically, CCL2 carried by the exosomes activates the PI3K/AKT/mTOR/HIF-1α signaling axis in endothelial cells via ACKR1, an effect abolished by CCL2 neutralization or ACKR1 knockdown. Together, these results demonstrate that the CCL2-positive ADSC subpopulation exerts multi-cellular and multi-target therapeutic actions, and that exosomes derived from this subpopulation offer a potent cell-free strategy to enhance diabetic wound healing by improving vascularization, modulating immune responses, and supporting ECM remodeling. - Source: PubMed
Zhao SongyunChen WanyingLiu KaiboXie JiahengChen YanmingDai HaoLu ZhongqiuChen LongwangHe YucangYu HuaLi Liqun - Colony-stimulating factor 1 receptor (CSF1R) is a key regulator of macrophage-driven liver inflammation. Here, we report a series of CSF1R inhibitors discovered through a structure-guided optimization strategy for the acute-phase treatment of acetaminophen-induced liver injury. For instance, compound exhibited potent CSF1R inhibition, a kinome-wide selective profile, and low cellular cytotoxicity. rapidly suppressed M-CSF-induced phosphorylation events and downstream signaling in macrophages. In an acute liver injury model, therapeutic administration of during the early inflammatory phase markedly reduced serum transaminase levels, improved hepatic histopathology, and alleviated inflammatory cell infiltration, accompanied by suppression of hepatic -CSF1R/p-AKT/p-ERK signaling and decreased levels of circulating TNF-α and IL-6. Collectively, these results support pharmacologic CSF1R blockade as a timely strategy to modulate macrophage-mediated inflammation in acute liver injury and warrant further preclinical development of . - Source: PubMed
Publication date: 2026/04/23
Yuan XueLiu KongjunZou YurongWei YuhanLiu QianhuanZheng GuoliRu MiaoZhang YuandongXiong BaojianGao JianmeiChen YongGong Qihai - - Source: PubMed
Publication date: 2026/04/22
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