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
Human colostrum: identification of minor proteins in the aqueous phase by proteomics.
Large-scale proteomics and phosphoproteomics of urinary exosomes.
Proteomic analysis of microvesicles from plasma of healthy donors reveals high individual variability.
In-depth proteomic analyses of exosomes isolated from expressed prostatic secretions in urine.
Extracellular matrix remodelling in response to venous hypertension: proteomics of human varicose veins.
Glycoproteomics Reveals Decorin Peptides With Anti-Myostatin Activity in Human Atrial Fibrillation.
Amino acid sequence of human plasma alpha 1B-glycoprotein: homology to the immunoglobulin supergene family.
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A1BG was purified from human plasma and completely sequenced, establishing it as a circulating plasma protein of unknown function.
"The complete amino acid sequence has been determined for alpha 1B-glycoprotein (alpha 1B), a protein of unknown function present in human plasma."
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The protein is built from five repeated immunoglobulin-like structural domains arising by internal duplication, placing it in the immunoglobulin supergene family.
"consists of five repeating structural domains, each containing about 95 amino acids and one disulfide bond"
Cysteine-rich secretory protein 3 is a ligand of alpha1B-glycoprotein in human plasma.
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CRISP3 circulates in human plasma bound to A1BG; the complex is specific, noncovalent, 1:1 and of nanomolar affinity.
"We demonstrate that CRISP-3 is a specific and high-affinity ligand of A1BG with a dissociation constant in the nanomolar range as evidenced by surface plasmon resonance."
A liver specific gene that is expressed in growth hormone transgenic mice and in normal female mice as a function of age.
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Mouse A1bg ("cDNA #5") was isolated as a transcript induced in the liver of growth hormone transgenic mice and absent from GH-deficient, GH-antagonist and GH-receptor-knockout mice, showing that its expression requires an intact GH-GH receptor axis.
"These findings suggest that induction of mRNA #5 in the liver requires a continuous pattern of GH secretion and an intact GH-GH receptor-signaling complex."
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The encoded protein has five immunoglobulin-related domains and is similar to rat and human alpha-1-B glycoprotein, an acidic serum protein of unknown function.
"P5 has five immunoglobulin related domains thus allowing it to be classified as a member of the immunoglobulin super family (IGSF)."
Alpha-1-B glycoprotein (A1BG) inhibits sterol-binding and export by CRISP2.
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Recombinant A1BG binds CRISP2 and prevents its cholesterol-sulfate binding; A1BG alone does not bind that sterol. Yeast CAP-dependent sterol export falls by more than 50%, while palmitate binding and fatty-acid export remain intact. Ig-domain-3 binding and magnesium dependence are experimentally examined.
"this binding is blocked in the presence of A1BG, which by itself does not bind cholesterol sulfate"
Sex-specific response to A1BG loss results in female dilated cardiomyopathy.
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Conditional cardiomyocyte deletion of A1bg in mice causes dilated cardiomyopathy in females but not males, indicating a sex-specific cardiac requirement.
"The glycoprotein A1BG has emerged as a female-specific regulator of cardiac structure and integrity"
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A1BG/tropomyosin co-immunostaining of adult mouse hearts places A1BG at atrial cardiomyocyte surfaces (Fig. 4D). This directly contradicts an exclusive-soluble-location argument.
"A1BG is associated with the outer surface of atrial CMs."
Adipocytes Promote Cisplatin Resistance through Secreting A1BG and Regulating NAMPT/PARP1 Axis-Mediated DNA Repair in Osteosarcoma.
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In osteosarcoma models, co-immunoprecipitation and colocalization support A1BG-NAMPT association. A1BG depletion reduces NAMPT protein stability; cycloheximide chase and lysosomal inhibitor rescue implicate turnover. These cell assays do not establish purified binary binding or specifically stabilization of extracellular NAMPT.
"Co‐IP followed by western blot analysis confirmed a robust interaction between A1BG and NAMPT"
Exocytosis of platelet alpha granule contents
Exocytosis of secretory granule lumen proteins
Exocytosis of ficolin-rich granule lumen proteins
Affinage mechanistic annotation for A1BG (human)
OpenScientist focused assessment of A1BG membrane, receptor and growth-hormone capacities
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The report computes a low mature-chain hydropathy maximum, corroborating absence of a conventional canonical transmembrane helix; it does not test all membrane associations.
"maximum hydropathy score was
**0.98**"
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The report asserts that structural evidence closes both receptor and membrane-pool routes. The membrane-pool exclusion is overturned by the mouse surface experiment, without establishing human receptor activity.
"structure closes the receptor and
membrane-pool routes"
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The report correctly identifies GH-dependent expression as insufficient by itself to demonstrate signaling work, but cannot independently verify the complete source assay record.
"High for transcriptional dependence; does not test protein signaling"
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The report admits that its PAINT topology was inferred from family membership rather than independently traced; the actual target lineage must govern propagation review.
"PANTHER tree topology (PTN nodes) inferred from family membership, not traced node-by-node."
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The report treats NAMPT stabilization as an extracellular interaction; the primary assays concern cellular NAMPT abundance and association, without proving a purified binary complex.
"Both documented functions are extracellular
protein-protein interactions."
A1BG hydropathy artifact recheck
A1BG focused report assessment