Entity Details

Primary name DMBT1
Entity type gene
Source Source Link

Details

PrimaryID1755
RefseqGeneNG_012644
SymbolDMBT1
Namedeleted in malignant brain tumors 1
Chromosome10
Location10q26.13
TaxID9606
Statuslive
SourceGenomegenomic
SourceOriginnatural
CreationDate1998-08-27
ModificationDate2021-06-20

Ontological Relatives

UniProt IDsDMBT1_HUMAN

GO terms

Show/Hide Table
GOName
GO:0001530 lipopolysaccharide binding
GO:0003677 DNA binding
GO:0005044 scavenger receptor activity
GO:0005576 extracellular region
GO:0005615 extracellular space
GO:0005737 cytoplasm
GO:0006898 receptor-mediated endocytosis
GO:0006952 defense response
GO:0007275 multicellular organism development
GO:0015031 protein transport
GO:0016032 viral process
GO:0019898 extrinsic component of membrane
GO:0030670 phagocytic vesicle membrane
GO:0030855 epithelial cell differentiation
GO:0031012 extracellular matrix
GO:0035375 zymogen binding
GO:0038187 pattern recognition receptor activity
GO:0042494 detection of bacterial lipoprotein
GO:0042589 zymogen granule membrane
GO:0043152 induction of bacterial agglutination
GO:0044267 cellular protein metabolic process
GO:0045087 innate immune response
GO:0048306 calcium-dependent protein binding
GO:0050829 defense response to Gram-negative bacterium
GO:0050830 defense response to Gram-positive bacterium
GO:0050840 extracellular matrix binding
GO:0051607 defense response to virus
GO:0061844 antimicrobial humoral immune response mediated by antimicrobial peptide
GO:0070062 extracellular exosome
GO:0070891 lipoteichoic acid binding
GO:1904399 heparan sulfate binding

Diseases

Show/Hide Table
Disease IDSourceNameDescription
137800 OMIMGlioma (GLM)Gliomas are benign or malignant central nervous system neoplasms derived from glial cells. They comprise astrocytomas and glioblastoma multiforme that are derived from astrocytes, oligodendrogliomas derived from oligodendrocytes and ependymomas derived from ependymocytes. The gene represented in this entry is involved in disease pathogenesis. Homozygous deletions may be the predominant mechanism of DMBT1 inactivation playing a role in carcinogenesis. DMBT1 is deleted in medulloblastoma and glioblastoma cell lines; point mutations have also been reported in patients with glioma. A loss or reduction of DMBT1 expression has been seen in esophageal, gastric, lung and colorectal carcinomas as well.