Entity Details

Primary name GPNMB_HUMAN
Entity type UniProt
Source Source Link

Details

AccessionQ14956
EntryNameGPNMB_HUMAN
FullNameTransmembrane glycoprotein NMB
TaxID9606
Evidenceevidence at protein level
Length572
SequenceStatuscomplete
DateCreated1997-11-01
DateModified2021-06-02

Ontological Relatives

GenesGPNMB

GO terms

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GOName
GO:0001818 negative regulation of cytokine production
GO:0001934 positive regulation of protein phosphorylation
GO:0005178 integrin binding
GO:0005886 plasma membrane
GO:0005887 integral component of plasma membrane
GO:0007155 cell adhesion
GO:0007165 signal transduction
GO:0007267 cell-cell signaling
GO:0008201 heparin binding
GO:0008285 negative regulation of cell population proliferation
GO:0016021 integral component of membrane
GO:0030335 positive regulation of cell migration
GO:0031901 early endosome membrane
GO:0031954 positive regulation of protein autophosphorylation
GO:0033162 melanosome membrane
GO:0034103 regulation of tissue remodeling
GO:0042056 chemoattractant activity
GO:0042130 negative regulation of T cell proliferation
GO:0045545 syndecan binding
GO:0045765 regulation of angiogenesis
GO:0048018 receptor ligand activity
GO:0050868 negative regulation of T cell activation
GO:0050918 positive chemotaxis
GO:0070374 positive regulation of ERK1 and ERK2 cascade
GO:1901215 negative regulation of neuron death
GO:2000134 negative regulation of G1/S transition of mitotic cell cycle

Subcellular Location

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Subcellular Location
Cell membrane
Early endosome membrane
Melanosome membrane

Domains

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DomainNameCategoryType
IPR000601 PKD domainDomainDomain
IPR013783 Immunoglobulin-like foldFamilyHomologous superfamily
IPR022409 PKD/Chitinase domainDomainDomain
IPR035986 PKD domain superfamilyFamilyHomologous superfamily

Diseases

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Disease IDSourceNameDescription
617920 OMIMAmyloidosis, primary localized cutaneous, 3 (PLCA3)A primary amyloidosis characterized by localized cutaneous amyloid deposition. This condition usually presents with itching (especially on the lower legs) and visible changes of skin hyperpigmentation and thickening that may be exacerbated by chronic scratching and rubbing. Primary localized cutaneous amyloidosis is often divided into macular and lichen subtypes although many affected individuals often show both variants coexisting. Lichen amyloidosis characteristically presents as a pruritic eruption of grouped hyperkeratotic papules with a predilection for the shins, calves, ankles and dorsa of feet and thighs. Papules may coalesce to form hyperkeratotic plaques that can resemble lichen planus, lichen simplex or nodular prurigo. Macular amyloidosis is characterized by small pigmented macules that may merge to produce macular hyperpigmentation, sometimes with a reticulate or rippled pattern. In macular and lichen amyloidosis, amyloid is deposited in the papillary dermis in association with grouped colloid bodies, thought to represent degenerate basal keratinocytes. The amyloid deposits probably reflect a combination of degenerate keratin filaments, serum amyloid P component, and deposition of immunoglobulins. PLCA3 inheritance is autosomal recessive. The disease is caused by variants affecting the gene represented in this entry.

Drugs

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DrugNameSourceType
DB05996 Glembatumumab vedotinDrugbankbiotech