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RING1 inhibits transactivation of RBP-J by Notch through interaction with LIM protein KyoT2The PcG protein HPC2 inhibits RBP-J-mediated transcription by interacting with LIM protein KyoT2Activation-induced cytidine deaminase expression in CD4+ T cells is associated with a unique IL-10-producing subset that increases with ageDisruption of Notch signaling aggravates irradiation-induced bone marrow injury, which is ameliorated by a soluble Dll1 ligand through Csf2rb2 upregulationFHL1C induces apoptosis in Notch1-dependent T-ALL cells through an interaction with RBP-J.Foxp3(+) T cells regulate immunoglobulin a selection and facilitate diversification of bacterial species responsible for immune homeostasis.Blocking Notch signal in myeloid cells alleviates hepatic ischemia reperfusion injury by repressing the activation of NF-κB through CYLDForced Activation of Notch in Macrophages Represses Tumor Growth by Upregulating miR-125a and Disabling Tumor-Associated Macrophages.The LIM domain protein FHL1C interacts with tight junction protein ZO-1 contributing to the epithelial-mesenchymal transition (EMT) of a breast adenocarcinoma cell line.Overexpression of Notch ligand Dll1 in B16 melanoma cells leads to reduced tumor growth due to attenuated vascularization.The transcriptional repression activity of KyoT2 on the Notch/RBP-J pathway is regulated by PIAS1-catalyzed SUMOylation.Metabolic shift induced by systemic activation of T cells in PD-1-deficient mice perturbs brain monoamines and emotional behavior.Cytotherapy with M1-polarized macrophages ameliorates liver fibrosis by modulating immune microenvironment in mice.Myeloid-Specific Blockade of Notch Signaling by RBP-J Knockout Attenuates Spinal Cord Injury Accompanied by Compromised Inflammation Response in Mice.Canonical notch pathway protects hepatocytes from ischemia/reperfusion injury in mice by repressing reactive oxygen species production through JAK2/STAT3 signaling.Myeloid-specific targeting of Notch ameliorates murine renal fibrosis via reduced infiltration and activation of bone marrow-derived macrophage.Crosstalk between hepatic tumor cells and macrophages via Wnt/β-catenin signaling promotes M2-like macrophage polarization and reinforces tumor malignant behaviorsMyeloid-specific disruption of recombination signal binding protein Jκ ameliorates hepatic fibrosis by attenuating inflammation through cylindromatosis in miceNotch Signaling Modulates Macrophage Polarization and Phagocytosis Through Direct Suppression of Signal Regulatory Protein α ExpressionNOTCH Signaling via WNT Regulates the Proliferation of Alternative, CCR2-Independent Tumor-Associated Macrophages in Hepatocellular Carcinoma
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P50
description
researcher ORCID ID = 0000-0003-1038-7037
@en
wetenschapper
@nl
name
Hongyan Qin
@ast
Hongyan Qin
@en
Hongyan Qin
@es
Hongyan Qin
@nl
type
label
Hongyan Qin
@ast
Hongyan Qin
@en
Hongyan Qin
@es
Hongyan Qin
@nl
altLabel
Qin H
@en
prefLabel
Hongyan Qin
@ast
Hongyan Qin
@en
Hongyan Qin
@es
Hongyan Qin
@nl
P106
P2798
P31
P496
0000-0003-1038-7037