AMY2B
Alpha-amylase 2B
Also known as: AMY2, AMY2B_HUMAN
Cross-references: UniProt · Ensembl · Human Protein Atlas · GeneCards · NCBI Gene
Protein identityUniProt · HPA
- UniProt accession
- P19961
- Gene
- AMY2B
- Ensembl
- ENSG00000240038
- Chromosome
- 1
- Canonical length
- 511 aa
- Protein class
- Enzymes, Metabolic proteins, Plasma proteins, Predicted secreted proteins
- Subcellular location
- Golgi apparatus,Cytosol
- Secretome location
- Secreted to digestive system
OverviewNCBI Gene
Amylases are secreted proteins that hydrolyze 1,4-alpha-glucoside bonds in oligosaccharides and polysaccharides, and thus catalyze the first step in digestion of dietary starch and glycogen. The human genome has a cluster of several amylase genes that are expressed at high levels in either salivary gland or pancreas. This gene encodes an amylase isoenzyme produced by the pancreas. [provided by RefSeq, Jun 2013]
Canonical amino-acid sequenceUniProt
511 residues, UniProt reviewed canonical sequence.
>P19961|AMY2B
1 MKFFLLLFTI GFCWAQYSPN TQQGRTSIVH LFEWRWVDIA LECERYLAPK GFGGVQVSPP
61 NENVAIHNPF RPWWERYQPV SYKLCTRSGN EDEFRNMVTR CNNVGVRIYV DAVINHMSGN
121 AVSAGTSSTC GSYFNPGSRD FPAVPYSGWD FNDGKCKTGS GDIENYNDAT QVRDCRLVGL
181 LDLALEKDYV RSKIAEYMNH LIDIGVAGFR LDASKHMWPG DIKAILDKLH NLNSNWFPAG
241 SKPFIYQEVI DLGGEPIKSS DYFGNGRVTE FKYGAKLGTV IRKWNGEKMS YLKNWGEGWG
301 FMPSDRALVF VDNHDNQRGH GAGGASILTF WDARLYKMAV GFMLAHPYGF TRVMSSYRWP
361 RQFQNGNDVN DWVGPPNNNG VIKEVTINPD TTCGNDWVCE HRWRQIRNMV NFRNVVDGQP
421 FTNWYDNGSN QVAFGRGNRG FIVFNNDDWT FSLTLQTGLP AGTYCDVISG DKINGNCTGI
481 KIYVSDDGKA HFSISNSAED PFIAIHAESK LLocalizationUniProt · AlphaFold · HPA
Whether an antibody against AMY2B can act on the native protein depends on physical access: surface and secreted proteins are reachable by circulating antibodies, intracellular proteins usually are not.
- Antibody reachability
- Secreted
- Secreted
- Yes
- Transmembrane segments
- 0
- Mean surface accessibility (rSASA)
- 0.2
- Highest tissue expression
- 33,017 nTPM
Expression across tissuesHPA
Tissue
- pancreas: 33,017 nTPM
- salivary gland: 257 nTPM
- retina: 72 nTPM
- skeletal muscle: 64 nTPM
- thyroid gland: 45 nTPM
- skin: 44 nTPM
Single-cell type
- pancreatic acinar cells: 2,812 nCPM
- myonuclei: 160 nCPM
- distal convoluted tubule cells: 152 nCPM
- cardiomyocytes: 60 nCPM
- rod photoreceptor cells: 53 nCPM
- cone photoreceptor cells: 50 nCPM
Immune cell
- classical monocyte: 5.3 nTPM
- intermediate monocyte: 2.7 nTPM
- non-classical monocyte: 2.4 nTPM
- myeloid DC: 1.7 nTPM
- neutrophil: 1.3 nTPM
- total PBMC: 1.3 nTPM
Brain region
- cerebellum: 61 nTPM
- basal ganglia: 50 nTPM
- cerebral cortex: 41 nTPM
- thalamus: 40 nTPM
- white matter: 39 nTPM
- amygdala: 38 nTPM
Genetic constraint and essentialitygnomAD · DepMap
Does the body need this protein intact? Low LOEUF or a strong DepMap dependency means loss or blockade of the protein is likely to be felt.
- gnomAD LOEUF (loss-of-function intolerance)
- 1.72
- gnomAD pLI
- 0
- gnomAD missense Z
- -2.52
Cancer expressionTCGA
Across TCGA tumor cohorts, this protein is over-expressed in roughly 4% of surveyed tumor types (aggregate summary; per-cohort expression, alteration, and survival load in the interactive view).
OntologyGO
Biological processes
Molecular functions
Cellular components
Protein domainsUniProt · Pfam · InterPro
KeywordsUniProt
Antibody and autoantibody relevanceSeroatlas analysis
Seroatlas reads AMY2B as an antibody target. Whether an autoantibody or antibody against AMY2B could matter depends on whether native AMY2B is physically reachable, whether the body needs it intact, and whether it acts in a disease-relevant tissue.
AMY2B is annotated as secreted, so native AMY2B circulates and is directly accessible to antibodies. Secreted and cell-surface proteins are the autoantibody targets most likely to act like drugs, blocking or depleting the native protein.
Annotation status
The present source text does not explicitly label AMY2B as an autoantigen. Seroatlas presents hypothesis context only and does not manufacture a known-serology claim.
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