Anti-Mouse CD11c FITC 500 ug
- Known as:
- Antibody toMouse CD11c fluorecein 500 ug
- Catalog number:
- 11-0114-85
- Category:
- -
- Supplier:
- eBioscience
- Gene target:
- Anti-Mouse CD11c FITC 500
Related genes to: Anti-Mouse CD11c FITC 500 ug
- Gene:
- ITGAX NIH gene
- Name:
- integrin subunit alpha X
- Previous symbol:
- CD11C
- Synonyms:
- CD11c
- Chromosome:
- 16p11.2
- Locus Type:
- gene with protein product
- Date approved:
- 1988-08-15
- Date modifiied:
- 2015-12-15
Related products to: Anti-Mouse CD11c FITC 500 ug
Related articles to: Anti-Mouse CD11c FITC 500 ug
- A consequence of neuroinflammation after traumatic brain injury (TBI) is microglial priming and increased sensitivity to secondary challenges including stressors and infections. We investigated whether diffuse TBI was associated with hypothalamic microglial morphological remodeling and altered inflammatory and neuroendocrine responses to a stressor, Acute Social Defeat (ASD). Adult male mice were subjected to diffuse TBI (midline fluid percussion injury) and then were exposed to acute stress (ASD for 2 h) 14 days later. Mice that received both TBI and ASD had increased mRNA expression of several cytokines and chemokines (Il1b, Il6 and Ccl2), receptors (Tlr4 and Itgax) and inflammatory pathways (Nfkb1) in periventricular hypothalamus and the pituitary gland. In addition, neurohormones (Avp and Oxt) were increased by ASD in the TBI mice. CRH immunoreactivity in the hypothalamic paraventricular nucleus (PVN) increased 20 h after ASD in mice with TBI. In behavioral testing, ASD provoked aversion to new objects in the TBI mice. PVN microglial morphological analysis revealed decreased cell size and complexity in mice exposed to TBI and ASD, indicating that ASD and TBI converged to increase microglial morphological remodeling in the hypothalamus. Although these results do not demonstrate that TBI induces microglial priming and sensitization of the hypothalamic stress response, they support that diffuse TBI is associated with changes in the hypothalamus that contribute to an altered response to acute stress, including an amplified neuroinflammatory response, microglial morphological remodeling, alterations in hypothalamic neuroendocrine markers and avoidance-like/anxiety-like behavior. Thus, TBI represents a risk factor for disrupted responses to acute stressors. - Source: PubMed
Publication date: 2026/08/18
León-Rodríguez AnaWangler LyndeGoodman EthanPacker JonathanDavis AmaraSheridan JohnGrondona Jesús MGodbout Jonathan PLópez-Ávalos María D - Feedback mechanisms regulate immune activation and prevent excessive tissue damage. TNFAIP3, also known as A20, serves as a crucial brake on inflammation, and mutations or haploinsufficiency of this gene are linked to diseases characterized by inappropriate inflammation. In this study, we document highly conserved patterns of cell type-specific gene expression, regulation, and induction of , and employ transgenic and gnotobiotic mouse models to investigate how adaptive immunity and the gut microbiome contribute to pathology arising from impaired A20 function. Contrary to our expectations, systemic inflammation resulting from deficiency in CD11c ()-expressing cells developed independently of autoreactive antibodies, B cells, and T cells. The microbiome also proved dispensable for disease manifestations in these models. These findings suggest that in diseases caused by insufficient TNFAIP3/A20 activity, autoantibodies may reflect a downstream consequence of disease rather than a causative driver, suggesting autoinflammatory rather than autoimmune pathology. These insights carry therapeutic implications for the treatment of -associated diseases. - Source: PubMed
Publication date: 2026/07/17
Van Damme Karel F AHertens PieterSichien DorineVan der Borght KatrienVan Moorleghem JustineDe Prijck SofieKlarenbeek AlexLouagie ElsLammens InésVanhee StijnVanhove ChristianDe Bleser PieterVan Laecke StevenDendooven AmélieHammad HamidaVereecke LarsElewaut Dirkvan Loo GeertLambrecht Bart N - infection-associated glomerulonephritis (SAGN) has emerged as the leading cause of infection-related glomerulonephritis (IRGN) in the Western subcontinents, but pathogenesis remains poorly understood in the absence of animal models and detailed molecular mechanisms. - Source: PubMed
Publication date: 2026/07/17
Karaiskos SpyrosSantana-Quintero LuisBott CherriPaul RahulBrodsky Sergey VAyoub IsabelleParikh Samir VRovin Brad HNadasdy TiborNakhasi Hira LGannavaram SreenivasSatoskar Anjali A - Acute myeloid leukemia (AML) features high biological heterogeneity and unfavorable prognoses, demanding reliable prognostic biomarkers. Dysregulated post-translational modifications (PTMs) drive AML progression by disrupting protein function and cellular signaling. This work constructed a PTM-based risk signature to predict AML survival and dissect the tumor immune microenvironment. - Source: PubMed
Publication date: 2026/07/23
Gan DonghuiZeng JinfangLin JunChen XiaojunHuang MengtingWeng DanYan Jun - Clear cell renal cell carcinoma (ccRCC) is a prevalent malignancy, representing 80-90% of kidney cancer cases. This study aimed to identify potential prognostic genes to improve patient survival prediction and provide new insights into the pathogenesis and treatment of ccRCC through comprehensive whole transcriptome sequencing analysis. - Source: PubMed
Publication date: 2026/07/08
Chang PengchengQin ZitongLiu RunzhangWang BinxianLu HuaiquanJing SuoshiGuo ChenhaoLi Weiping