Gene Ontology annotation through association of InterPro records with GO terms
Annotation inferences using phylogenetic trees
Gene Ontology annotation based on UniProtKB/Swiss-Prot Subcellular Location vocabulary mapping, accompanied by conservative changes to GO terms applied by UniProt
The LDL receptor-related protein LRP6 mediates internalization and lethality of anthrax toxin.
Anthrax toxin receptor 1/tumor endothelium marker 8 mediates cell spreading by coupling extracellular ligands to the actin cytoskeleton.
-
Extracellular attachment and cytoplasmic actin coupling contribute distinct parts of receptor-mediated spreading.
"the extracellular and transmembrane domains of TEM8 were
sufficient to provide cell attachment, the intracellular domain was critical for
spreading."
Quantitative proteomics identifies a Dab2/integrin module regulating cell migration.
The cell surface structure of tumor endothelial marker 8 (TEM8) is regulated by the actin cytoskeleton.
-
External FLAG detection establishes a surface receptor pool despite masking of another antibody epitope.
"Immunofluorescence staining using anti-FLAG mAbs revealed FLAG-TEM8 on the cell surface of non-permeabilized 293/FlagT8 cells immediately following transfection"
TEM8 functions as a receptor for uPA and mediates uPA-stimulated EGFR phosphorylation.
-
uPA binding is associated with receptor phosphorylation and EGFR/ERK responses in the tested cellular setting.
"Binding of
uPA stimulated the phosphorylation of TEM8 and augmented phosphorylation of EGFR
and ERK1/2."
ANTXR1-bound pagA(197-794) forms oligomers
cya and lef bind to pagA(197-794):ANTXR1 oligomer
Furin cleaves ANTXR1-bound pagA to yield pagA(197-794)
Endocytosis of cya:lef:(pagA(197-794):ANTXR1 oligomer) (plasma membrane to endosome membrane)
pagA(197-794):ANTRX1 oligomer transports cya and lef (target cell endosome to cytosol)
ANTXR1 primary-source assessment and annotation review notes
Direct interaction between anthrax toxin receptor 1 and the actin cytoskeleton.
-
A synthetic human cytoplasmic tail segment binds purified human beta-actin and bundles preformed filaments; monomer-associated aggregates do not establish polymerization.
"These data suggest this region of the cytoplasmic tail of ANTXR1 bundles filamentous actin."
Mutations in ANTXR1 cause GAPO syndrome.
-
Biallelic ANTXR1 variants in affected human families establish the GAPO disease association.
"identified homozygous nonsense mutations (c.262C>T [p.Arg88*]
and c.505C>T [p.Arg169*]) or splicing mutations (c.1435-12A>G
[p.Gly479Phefs*119]) in ANTXR1, which encodes anthrax toxin receptor 1."
Lack of evidence for a role of anthrax toxin receptors as surface receptors for collagen VI and for its cleaved-off C5 domain/endotrophin.
-
Murine ANTXR1/2 constructs did not increase binding of assembled collagen VI under the tested conditions; NG2 served as a positive cell-binding control.
"overexpression of the two anthrax toxin receptors did not increase the interaction of collagen VI with the cells."
Cancer cell survival depends on collagen uptake into tumor-associated stroma.
-
TEM8 fusion binding and MIDAS controls support collagen-I recognition, with an explicitly human receptor mutant series.
"WT TEM8-AP, but not TEM8-D150A-AP or AP alone, robustly bound PA and collagen I"
-
The tested TEM8 preparations also bound collagen VI in the reported ECM assay.
"Notably, TEM8 bound col1 and collagen VI, but not laminin or collagen IV"
ANTXR1 deficiency promotes fibroblast senescence: implications for GAPO syndrome as a progeroid disorder.
-
ANTXR1 loss produces senescence-associated phenotypes in tested human fibroblasts; this supplies disease context rather than a new direct senescence-process assertion.
"ANTXR1 deficiency initiates
a senescent phenotype in human fibroblasts"