IGF-1 induced HIF-1α-TLR9 cross talk regulates inflammatory responses in glioma.
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The Response of Macrophages and Neutrophils to Hypoxia in the Context of Cancer and Other Inflammatory DiseasesTargeting oncogenic ALK and MET: a promising therapeutic strategy for glioblastomaSimulation predicts IGFBP2-HIF1α interaction drives glioblastoma growthThe role of CXC-chemokine receptor CXCR2 and suppressor of cytokine signaling-3 (SOCS-3) in renal cell carcinoma.Immunohistochemical analysis of IL-6, IL-8/CXCR2 axis, Tyr p-STAT-3, and SOCS-3 in lymph nodes from patients with chronic lymphocytic leukemia: correlation between microvascular characteristics and prognostic significance.Recent advances in the role of toll-like receptors and TLR agonists in immunotherapy for human gliomaStratified control of IGF-I expression by hypoxia and stress hormones in osteoblasts.Bone resorption facilitates osteoblastic bone metastatic colonization by cooperation of insulin-like growth factor and hypoxia.TLR9 deficiency promotes CD73 expression in T cells and diabetes protection in nonobese diabetic mice.COL3A1 and SNAP91: novel glioblastoma markers with diagnostic and prognostic value.HIF-1 in cancer therapy: two decade long story of a transcription factor.Nuclear translocation of HIF-1α induced by influenza A (H1N1) infection is critical to the production of proinflammatory cytokinesIdentification of IGF-1-enhanced cytokine expressions targeted by miR-181d in glioblastomas via an integrative miRNA/mRNA regulatory network analysis.MiR-212-3p inhibits glioblastoma cell proliferation by targeting SGK3.A critical overview of long non-coding RNA in glioma etiology 2016: an update.FAT1 acts as an upstream regulator of oncogenic and inflammatory pathways, via PDCD4, in glioma cells.Metabolic Reprogramming in Glioma.Low TLR9 expression defines an aggressive subtype of triple-negative breast cancer.Age-dependent alterations to paraventricular nucleus insulin-like growth factor 1 receptor as a possible link between sympathoexcitation and inflammation.Hypoxia regulates Toll-like receptor-9 expression and invasive function in human brain cancer cells in vitro.Targeted deletion of miR-139-5p activates MAPK, NF-κB and STAT3 signaling and promotes intestinal inflammation and colorectal cancer.Migration/Invasion of Malignant Gliomas and Implications for Therapeutic Treatment.Hypoxia-derived exosomes induce putative altered pathways in biosynthesis and ion regulatory channels in glioblastoma cells.Matrine induces senescence of human glioblastoma cells through suppression of the IGF1/PI3K/AKT/p27 signaling pathway
P2860
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P2860
IGF-1 induced HIF-1α-TLR9 cross talk regulates inflammatory responses in glioma.
description
2011 nî lūn-bûn
@nan
2011年の論文
@ja
2011年論文
@yue
2011年論文
@zh-hant
2011年論文
@zh-hk
2011年論文
@zh-mo
2011年論文
@zh-tw
2011年论文
@wuu
2011年论文
@zh
2011年论文
@zh-cn
name
IGF-1 induced HIF-1α-TLR9 cross talk regulates inflammatory responses in glioma.
@en
IGF-1 induced HIF-1α-TLR9 cross talk regulates inflammatory responses in glioma.
@nl
type
label
IGF-1 induced HIF-1α-TLR9 cross talk regulates inflammatory responses in glioma.
@en
IGF-1 induced HIF-1α-TLR9 cross talk regulates inflammatory responses in glioma.
@nl
prefLabel
IGF-1 induced HIF-1α-TLR9 cross talk regulates inflammatory responses in glioma.
@en
IGF-1 induced HIF-1α-TLR9 cross talk regulates inflammatory responses in glioma.
@nl
P2093
P1433
P1476
IGF-1 induced HIF-1α-TLR9 cross talk regulates inflammatory responses in glioma
@en
P2093
Nitin Koul
Sanchari Sinha
Vivek Sharma
P304
P356
10.1016/J.CELLSIG.2011.06.024
P577
2011-07-03T00:00:00Z