IndraLab
Statements
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"Additionally, as shown in xref , the CellChat analysis revealed the presence of ligand receptors, including VEGFB-VEGFR1, NAMPT-INSR, and VEGFA-VEGFR1 ( xref – xref ) which play a crucial role in AS, all participate in communication between these two types of cells, underscoring the importance of their interaction in AS."
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"NPCs with high AA metabolic activity demonstrated the ability to engage in cellular communication with NPPCs through ANGPTL4–(ITGA5 + ITGB1), ANGPTL4–CDH11, ANGPTL4–SDC2, FGF2–FGR1, and PDGFC–PDGFRA interactions; with EC through ANGPTL4–(ITGA5 + ITGB1) and ANGPTL4–CDH5 interactions; and with Noto via ANGPTL4–(ITGA5 + ITGB1), ANGPTL4–SDC2, ANGPTL4–SDC3, ANGPTL4–SDC4, FGF2–FGFR1, NAMPT–(ITGA5 + ITGB1), and NAMPT–INSR interactions."
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"In addition, scRNA-seq and quantitative reverse transcription polymerase chain reaction (qRT-PCR) confirmed that the intercellular communication between secretory phosphoprotein 1 (SPP1)-cluster of differentiation (CD44), insulin-like growth factor (IGF)-1-IGF1r and visfatin-insulin receptor (Insr) associated with bone metabolism and insulin metabolism was increased and enhanced in the liver at 6 w post-infection."
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"Among them, fibroblasts, endothelial cells, and macrophages targeting GLY high malignant cells work together through certain tumor-promoting signaling pathways, including the NAMPT-(ITGA5 + IAGB1), SPP1-(ITGA5 + ITGB1), NAMPT-INSR, and TGFB1 (ACVR1B + TGFBR2) signaling pairs, which interact to mediate uncontrolled tumor proliferation and growth ( xref B)."
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"For example, the FGF pathway exerts the most of its effects on cells in SPG1 and SPG2 ( xref ), consistent with a prior observation. xref We also found that myoid cells are the major cell type to receive the signaling activities of the PDGF pathway (including LR pairs PDGFA-PDGFRA, PDGFA-PDGFRB, etc.) and VISFATIN pathway (NAMPT-INSR and NAMPT-ITGA5-ITGB1), while Sertoli cells receive the most of GAS (GAS6-AXL, GAS6-MERTK, and GAS6-TYRO3) signaling activities ( xref )."
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"To further elucidate the impact of MACs on malignant cells, we explored potential ligand‐receptor pairs and found NAMPT‐INSR, LGALS9‐SLC1A5, LGALS9‐CD47, LGALS9‐CD44, GRN‐SORT1, and CD46‐JAG1 are all significantly enriched in cell‐cell communication (Figure xref ; Figure xref , Supporting Information)."
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"Early studies suggested binding of extracellular NAMPT to the insulin receptor as a basis for its activity, however, these studies have since been retracted and no specific extracellular receptor has been identified to date. xref The presence of an NAMPT receptor signaling pathway has also been supported by the induction of IL‐6 by NAMPT in the presence of the inhibitor of NAMPT enzymatic activity FK‐866. xref In contrast, the role of NAMPT enzymatic activity in the pathogenesis of inflammatory arthritis has been supported by studies that demonstrated the role of cellular NAD regulation in lymphocyte development and activation. xref , xref This has been supported further by studies in the collagen‐induced arthritis mouse model that have found inhibition of NAMPT by either FK‐866 or siRNA‐based gene‐silencing inhibits leukocyte activation and infiltration, cytokine production, and overall disease progression. xref , xref Further supporting the role of NAMPT enzyme activity in disease progression, depletion of NAD levels in circulating leukocytes has been associated with the efficacy of FK‐866 in the collagen‐induced arthritis mouse model. xref "
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"Meng Zhou et al xref discovered that various signaling pathways, such as those involving VISTANT, SPP1, and IGF, as well as receptor-ligand pairs, including NRG1-ERBB4, SPP1-CD44, Igf1-Igf1r, and NAMPT-INSR, may play significant roles in DKD by inducing crosstalk between renal and immune cells."
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"In conclusion, our current study analyzed immune cells and inflammation-related pathways in DKD, further revealing that VISTANT, SPP1, GALECTIN and IGF signaling pathways and SPP1-CD44, NRG1-ERBB4, NAMPT-INSR, Sema3g (Nrp1+Plxna4), Igf1- Igf1r receptor ligand pairs might occupy an important place in the occurrence and progress of DKD."