Serum albumin precursor - Homo sapiens (Human)

Sequence

>P02768|ALBU_HUMAN Serum albumin precursor - Homo sapiens MKWVTFISLLFLFSSAYSRGVFRRDAHKSEVAHRFKDLGEENFKALVLIAFAQYLQQCPF EDHVKLVNEVTEFAKTCVADESAENCDKSLHTLFGDKLCTVATLRETYGEMADCCAKQEP ERNECFLQHKDDNPNLPRLVRPEVDVMCTAFHDNEETFLKKYLYEIARRHPYFYAPELLF FAKRYKAAFTECCQAADKAACLLPKLDELRDEGKASSAKQRLKCASLQKFGERAFKAWAV ARLSQRFPKAEFAEVSKLVTDLTKVHTECCHGDLLECADDRADLAKYICENQDSISSKLK ECCEKPLLEKSHCIAEVENDEMPADLPSLAADFVESKDVCKNYAEAKDVFLGMFLYEYAR RHPDYSVVLLLRLAKTYETTLEKCCAAADPHECYAKVFDEFKPLVEEPQNLIKQNCELFE QLGEYKFQNALLVRYTKKVPQVSTPTLVEVSRNLGKVGSKCCKHPEAKRMPCAEDYLSVV LNQLCVLHEKTPVSDRVTKCCTESLVNRRPCFSALEVDETYVPKEFNAETFTFHADICTL SEKERQIKKQTALVELVKHKPKATKEQLKAVMDDFAAFVEKCCKADDKETCFAEEGKKLV AASQAALGL

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Function	Serum albumin, the main protein of plasma, has a good binding capacity for water, Ca(2+), Na(+), K(+), fatty acids, hormones, bilirubin and drugs. Its main function is the regulation of the colloidal osmotic pressure of blood.
Subcellular location	Secreted.
Tissue specificity	Plasma.
Post-translational modification	Kenitra variant is partially O-glycosylated at Thr-620. It has two new disulfide bonds Cys-600 to Cys-602 and Cys-601 to Cys-606. Glycated in diabetic patients.
Polymorphism	The sequence shown is that of variant albumin A.
Involvement in disease	Defects in ALB are a cause of familial dysalbuminemic hyperthyroxinemia (FDH) [MIM:103600]. FDH is a form of euthyroid hyperthyroxinemia that is due to increased affinity of ALB for T(4). It is the most common cause of inherited euthyroid hyperthyroxinemia in Caucasian population. A variant structure of albumin could lead to increased binding of zinc resulting in an asymptomatic augmentation of zinc concentration in the blood [MIM:194470].
Miscellaneous	Acetylated on Lys-223 by acetylsalicylic acid.
Sequence similarities	Belongs to the ALB/AFP/VDB family. Contains 3 albumin domains.
Caution	A peptide arising from positions 166 to 174 was originally (Ref.23 and Ref.24) termed neurotensin-related peptide (NRP) or kinetensin and was thought to regulates fat digestion, lipid absorption, and blood flow.

Keywords
Cellular component	Secreted
Coding sequence diversity	Alternative splicing Polymorphism
Disease	Disease mutation
Domain	Repeat Signal
Ligand	Copper Lipid-binding Metal-binding
PTM	Cleavage on pair of basic residues Glycation Glycoprotein
Technical term	3D-structure Direct protein sequencing
Gene Ontology (GO)
Biological process	cellular response to starvation Inferred from direct assay. Source: UniProtKB hemolysis by symbiont of host red blood cells Inferred from direct assay. Source: UniProtKB maintenance of mitochondrion location Inferred from direct assay. Source: UniProtKB negative regulation of apoptosis Inferred from direct assay. Source: UniProtKB negative regulation of non-apoptotic programmed cell death Non-traceable author statement. Source: UniProtKB transport Traceable author statement. Source: UniProtKB
Cellular component	extracellular region Non-traceable author statement. Source: UniProtKB platelet alpha granule lumen Inferred from Experiment. Source: Reactome protein complex Inferred from direct assay. Source: UniProtKB
Molecular function	DNA binding Inferred from direct assay. Source: UniProtKB antioxidant activity Non-traceable author statement. Source: UniProtKB copper ion binding Non-traceable author statement. Source: UniProtKB drug binding Ref.38 Inferred from direct assay. Source: UniProtKB fatty acid binding Ref.36 Inferred from direct assay. Source: UniProtKB protein binding Inferred from physical interaction. Source: UniProtKB pyridoxal phosphate binding Inferred from direct assay. Source: UniProtKB toxin binding Inferred from direct assay. Source: UniProtKB
Complete GO annotation...

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Amino acid modifications

Natural variations