IndraLab
Statements
sparser
"We also observed potential interacting pairs between EP_C1_LMP1 cells with activated Notch pathway and multiple cell types through NOTCH1-TNF and NOTCH2-JAG2, which have been related to radiation sensitivity xref and cancer stem-like side population cells xref in NPC (Supplementary Fig. xref )."
sparser
"We observed that, some classical signaling such as TNF-NOTCH1 pair was expressed in all eight gained ImC-LSC, as reported, Notch and TNF signaling had all been verified to regulate the homeostasis of the corneal epithelium and the corneal inflammatory response and wound healing after injury [ xref – xref ]."
sparser
"Next, we found that non-HBV T/NK cells had the strongest proinflammatory cytokine interactions with myeloid clusters via the IFNG-IFNGR1, TNF-TNFRSF1B, TNF-VSIR, TNF-TNFRSF1A, TNF-NOTCH1, and TNF-SEMA4C axes, suggesting that IFNG and TNF activated myeloid cells xref (Fig. xref )."
sparser
"For the receptor-ligand interaction, Agrafioti et al. [ xref ] found that PVR-TIGIT, PVR-CD96, and PV-CD226 receptor/ligand pairs interact between M1 and T cells, while TNF-NOTCH1 and PVR-TNFSF9 receptor/ligand pairs interact between M1 and B cells, and many other cross-talks were enhanced in periodontitis-affected sites."
reach
"By linking Notch and TNFalpha it was shown that (1) Notch-1 mucosal expression differs in inflamed and non inflamed mucosa and increases in response to anti-TNFalpha treatment; (2) Notch-1 function is regulated by TNFalpha inhibitors; (3) Notch-1 binds to TNFalpha; and (4) Notch-1 inhibition prevents anti-TNFalpha-induced T cell cycle arrest but not apoptosis."
sparser
"By linking Notch and TNFα it was shown that (1) Notch-1 mucosal expression differs in inflamed and non-inflamed mucosa and increases in response to anti-TNFα treatment; (2) Notch-1 function is regulated by TNFα inhibitors; (3) Notch-1 binds to TNFα; and (4) Notch-1 inhibition prevents anti-TNFα-induced T cell cycle arrest but not apoptosis."
sparser
"CellphoneDB analysis revealed that the ligands (WNT5A, PDGFB, IGF1, PROS1, OSM, and TNF) were specifically expressed in MES-MDM 1 and 2 ( xref A and B) and suggested an enhanced interaction of TNF-CELSR2, TNF-PTPRS, TNF-DAG1, TNF-SEMA4C, TNF-NOTCH1, TNF- RIPK1 between MES-MDM and MES/NPC-like cancer cells ( xref G and xref C)."