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Mouse (Murine) IL34 ELISA Kit for Sandwich ELISA - ABIN424215
Mizuno, Doi, Mizoguchi, Jin, Noda, Sonobe, Takeuchi, Suzumura: Interleukin-34 selectively enhances the neuroprotective effects of microglia to attenuate oligomeric amyloid-? neurotoxicity. in The American journal of pathology 2011
Show all 2 references for ABIN424215
Human IL34 ELISA Kit for Sandwich ELISA - ABIN415030
Li, Jin, Wu, Zhang, Hu, Cao, Chen: Increased serum interleukin-34 in patients with coronary artery disease. in The Journal of international medical research 2012
The receiver operating characteristic (ROC) curve analysis has shown that IL-34 has more discriminatory power than C-reactive protein (CRP (show CRP ELISA Kits)) for the risk of diabetic complications. The cut-off value for IL-34 was established as 91.2 pg/mL. The gist of our research was identification of IL-34 as an additional potential inflammatory biomarker for the prediction of the risk of vascular diabetic complications.
miR (show MLXIP ELISA Kits)-28-5p-IL-34-macrophage feedback loop modulates hepatocellular carcinoma metastasis
findings demonstrated that M-CSF (show CSF1 ELISA Kits) binds to IL-34; molecular docking studies predicted the formation of a heteromeric M-CSF (show CSF1 ELISA Kits)/IL-34 cytokine
These results suggest that IL-34, a novel osteoclastogenic cytokine, plays a role in rheumatoid arthritis-associated joint damage and is a potential biomarker for predicting subsequent radiographic progression in patients with RA.
IL-34 is expressed by human FOXP3 (show FOXP3 ELISA Kits)+CD45RCloCD8+ and CD4 (show CD4 ELISA Kits)+ Tregs and markedly inhibited alloreactive immune responses.
This paper provides evidence of alternative binding of IL-34 to chondroitin sulphates and syndecan-1 (show SDC1 ELISA Kits) at the cell surface that modulates M-CSFR (show CSF1R ELISA Kits) activation.
In vitro and in vivo experiments indicate that IL-34 expression is regulated by TNF-a (show TNF ELISA Kits) and IL-1b (show IL1B ELISA Kits) and that its overexpression is associated with an increase in osteosarcoma growth and metastasis.
the expression pattern of IL-34 in ileum and colon and suggest IL-34 as a new modulator of inflammation in inflammatory bowel disease
IL-34 is up-regulated in inflammatory bowel disease and suggest a role for this cytokine in sustaining the inflammatory responses in this disease
IL-34 is induced by IL-22 (show IL22 ELISA Kits) in the inflammatory cascade in response to IAV infection.
study concludes that Langerhans cells require IL-34 when residing in fully differentiated and anatomically intact skin epidermis, but rely on neutrophil-derived CSF1 (show CSF1 ELISA Kits) during inflammation
constitutive IL-34 expressed by skin keratinocytes might suppress resident macrophage responses to C. albicans colonisation by maintaining low levels TLR2 (show TLR2 ELISA Kits) and Dectin-1 (show CLEC7A ELISA Kits) expression by macrophages.
IL-34 protected blood-brain barrier integrity by restored expression levels of tight junction proteins, which were downregulated by pro-inflammatory cytokines.
IL-34-dependent, Mo-mediated, CSF-1 (show CSF1 ELISA Kits) nonredundant mechanisms promote persistent ischemia-incited AKI that worsens subsequent CKD.
Tumor necrosis factor-alpha (show TNF ELISA Kits) induces IL-34 expression via NF-kappaB (show NFKB1 ELISA Kits) in MC3T3-E1 osteoblastic cells.
These findings suggest that TGF-beta (show TGFB1 ELISA Kits) produced by IL-34-treated microglia is a negative regulator of microglial proliferation and enhances the neuroprotective property of microglia.
Differentiated signaling between IL-34 and CSF-1 (show CSF1 ELISA Kits) is likely achieved by the relative thermodynamic independence of IL-34 versus negative cooperativity of CSF-1 (show CSF1 ELISA Kits) at the CSF-1 receptor (show CSF1R ELISA Kits) recognition sites.
IL-34 as a nonredundant cytokine for the development of Langerhans cells during embryogenesis as well as for their homeostasis in the adult skin.
Interleukin-34 is a cytokine that promotes the differentiation and viability of monocytes and macrophages through the colony-stimulating factor-1 receptor (CSF1R\; MIM 164770) (Lin et al., 2008