Manual transfer of experimentally-verified manual GO annotation data to orthologs by curator judgment of sequence similarity
Annotation inferences using phylogenetic trees
Gene Ontology annotation based on UniProtKB/Swiss-Prot keyword mapping
Gene Ontology annotation based on UniProtKB/Swiss-Prot Subcellular Location vocabulary mapping, accompanied by conservative changes to GO terms applied by UniProt
Gene Ontology annotation based on curation of immunofluorescence data
Automatic transfer of experimentally verified manual GO annotation data to orthologs using Ensembl Compara
Automatic assignment of GO terms using logical inference, based on on inter-ontology links
Electronic Gene Ontology annotations created by ARBA machine learning models
Combined Automated Annotation using Multiple IEA Methods
HMGB1 and HMGB2 cell-specifically down-regulate the p53- and p73-dependent sequence-specific transactivation from the human Bax gene promoter.
Structural basis for the proinflammatory cytokine activity of high mobility group box 1.
Association of chromatin proteins high mobility group box (HMGB) 1 and HMGB2 with mitotic chromosomes.
Evidence for involvement of HMGB1 protein in human DNA mismatch repair.
The long acidic tail of high mobility group box 1 (HMGB1) protein forms an extended and flexible structure that interacts with specific residues within and between the HMG boxes.
Release of high mobility group box 1 by dendritic cells controls T cell activation via the receptor for advanced glycation end products.
Endogenous signals released from necrotic cells augment inflammatory responses to bacterial endotoxin.
HMGB1 is a cofactor in mammalian base excision repair.
Induction of immunological tolerance by apoptotic cells requires caspase-dependent oxidation of high-mobility group box-1 protein.
High mobility group protein-1 inhibits phagocytosis of apoptotic neutrophils through binding to phosphatidylserine.
Chromatin-specific remodeling by HMGB1 and linker histone H1 silences proinflammatory genes during endotoxin tolerance.
HMGB1 and HMGB2 proteins up-regulate cellular expression of human topoisomerase IIalpha.
Complementary quantitative proteomics reveals that transcription factor AP-4 mediates E-box-dependent complex formation for transcriptional repression of HDM2.
Effect of high mobility group box-1 protein on apoptosis of peritoneal macrophages.
Linking innate and adaptive immunity: human Vgamma9Vdelta2 T cells enhance CD40 expression and HMGB-1 secretion.
Endogenous HMGB1 regulates autophagy.
HMGB1 inhibits macrophage activity in efferocytosis through binding to the alphavbeta3-integrin.
Identification of lipopolysaccharide-binding peptide regions within HMGB1 and their effects on subclinical endotoxemia in a mouse model.
HMGB1 promotes recruitment of inflammatory cells to damaged tissues by forming a complex with CXCL12 and signaling via CXCR4.
HMGB1 conveys immunosuppressive characteristics on regulatory and conventional T cells.
Insights into RNA biology from an atlas of mammalian mRNA-binding proteins.
The mRNA-bound proteome and its global occupancy profile on protein-coding transcripts.
HMGB1-facilitated p53 DNA binding occurs via HMG-Box/p53 transactivation domain interaction, regulated by the acidic tail.
Emodin-6-O-β-D-glucoside inhibits HMGB1-induced inflammatory responses in vitro and in vivo.
High mobility group Box 1 inhibits human pulmonary artery endothelial cell migration via a Toll-like receptor 4- and interferon response factor 3-dependent mechanism(s).
Chaperone-like activity of high-mobility group box 1 protein and its role in reducing the formation of polyglutamine aggregates.
An immunogenic peptide in the A-box of HMGB1 protein reverses apoptosis-induced tolerance through RAGE receptor.
HMGB1-DNA complex-induced autophagy limits AIM2 inflammasome activation through RAGE.
A proteome-scale map of the human interactome network.
Cutting Edge: identification of neutrophil PGLYRP1 as a ligand for TREM-1.
AGEs and HMGB1 Increase Inflammatory Cytokine Production from Human Placental Cells, Resulting in an Enhancement of Monocyte Migration.
miR-193a-3p interaction with HMGB1 downregulates human endothelial cell proliferation and migration.
Architecture of the human interactome defines protein communities and disease networks.
Delineating the HMGB1 and HMGB2 interactome in prostate and ovary epithelial cells and its relationship with cancer.
Characterization of HMGB1/2 Interactome in Prostate Cancer by Yeast Two Hybrid Approach: Potential Pathobiological Implications.
A reference map of the human binary protein interactome.
Interactome Mapping Provides a Network of Neurodegenerative Disease Proteins and Uncovers Widespread Protein Aggregation in Affected Brains.
The HMGB1-2 Ovarian Cancer Interactome. The Role of HMGB Proteins and Their Interacting Partners MIEN1 and NOP53 in Ovary Cancer and Drug-Response.
Genome-wide CRISPR Screens Reveal Host Factors Critical for SARS-CoV-2 Infection.
Dual proteome-scale networks reveal cell-specific remodeling of the human interactome.
SARS-CoV-2 ORF3a induces RETREG1/FAM134B-dependent reticulophagy and triggers sequential ER stress and inflammatory responses during SARS-CoV-2 infection.
Multimodal cell maps as a foundation for structural and functional genomics.
The high mobility group protein HMG1 can reversibly inhibit class II gene transcription by interaction with the TATA-binding protein.
The nonspecific DNA-binding and -bending proteins HMG1 and HMG2 promote the assembly of complex nucleoprotein structures.
V(D)J recombination: modulation of RAG1 and RAG2 cleavage activity on 12/23 substrates by whole cell extract and DNA-bending proteins.
High mobility group protein-1 (HMG-1) is a unique activator of p53.
MyD88 forms a complex with TIRAP:activated TLR2/4
IRAK4 binds to the activated TLR receptor:TIRAP:MyD88 complex
IRAK1 or IRAK2 binds to the activated IRAK4 :activated TLR:MyD88:TIRAP complex
First phosphorylation of IRAK1 by IRAK4 bound to activated TLR:MyD88:Mal
Second phosphorylation of IRAK1 by IRAK4 bound to activated TLR:MyD88:TIRAP
Multiple IRAK1 autophosphorylation steps
Dissociation of hp-IRAK1:TRAF6 from the activated TLR:oligo-Myd88:TIRAP:p-IRAK4 complex
Activated TLR2/4 interacts with MAL (TIRAP)
TIRAP is phosphorylated by BTK
Dissociation of p-IRAK2:TRAF6 from the activated TLR:oligo-Myd88:TIRAP:p-IRAK4 complex
Activated TLR2/4:TIRAP interacts with BTK
Association of HMGB1/HMGB2 with chromatin
Defective IRAK4 does not bind MyD88:MAL:BTK:activated TLR2/4
Defective MyD88 does not oligomerize within the activated TLR2/4 complex
Defective MyD88 does not bind MAL(TIRAP):TLR2/4
Exocytosis of secretory granule lumen proteins
Exocytosis of ficolin-rich granule lumen proteins
Advanced glycosylation end product-specific receptor (AGER/RAGE) is a multiligand receptor
IRAK4 autophosphorylation in the complex with activated TLR:MyD88:TIRAP
Phosphorylation of IRAK2 bound to the activated IRAK4:MyD88 oligomer:TIRAP:activated TLR complex
MyD88 oligomerization within the complex of activated TLR:TIRAP:MyD88
Deep research report on HMGB1