Molecular weight (DA)
265kD
Immunogen
Synthesized peptide derived from part region of human protein
Specificity
DMBT1 Polyclonal Antibody detects endogenous levels of protein.
Formulation
Liquid in PBS containing 50% glycerol, and 0.02% sodium azide.
Dilution rate
IHC-p 1:50-300. IF 1:50-200
Purification process (Immunogen)
The antibody was affinity-purified from rabbit antiserum by affinity-chromatography using epitope-specific immunogen.
Background
Loss of sequences from human chromosome 10q has been associated with the progression of human cancers. This gene was originally isolated based on its deletion in a medulloblastoma cell line. This gene is expressed with transcripts of 6.0, 7.5, and 8.0 kb in fetal lung and with one transcript of 8.0 kb in adult lung, although the 7.5 kb transcript has not been characterized. The encoded protein precursor is a glycoprotein containing multiple scavenger receptor cysteine-rich (SRCR) domains separated by SRCR-interspersed domains (SID). Transcript variant 2 (8.0 kb) has been shown to bind surfactant protein D independently of carbohydrate recognition. This indicates that DMBT1 may not be a classical tumor suppressor gene, but rather play a role in the interaction of tumor cells and the immune system. [provided by RefSeq, Mar 2016],
Function
alternative products:More isoforms may exist,developmental stage:Expressed in fetal lung, intestine and skin. Secreted to the extracellular matrix (ECM) in certain fetal epithelia.,disease:A deletion allele of DMBT1 which lacks five of the SRCR domains is associated with an increased risk of Crohn disease.,disease:Defects in DMBT1 are the cause of glioma of the brain [MIM:137800]. Gliomas are central nervous system neoplasms derived from glial cells and comprise astrocytomas, glioblastoma multiforme, oligodendrogliomas, and ependymomas.,disease:Inactivation of DMBT1 plays an important role in carcinogenesis. A loss or reduction of DMBT1 expression was seen in esophageal, gastric, lung and colorectal carcinomas. Deleted in medulloblastoma and glioblastoma cell lines. Homozygous deletions may be the predominant mechanism of inactivation.,domain:The SRCR domains mediate binding to bacteria.
Protein name
Deleted in malignant brain tumors 1 protein (Glycoprotein 340) (Gp-340) (Hensin) (Salivary agglutinin) (SAG) (Surfactant pulmonary-associated D-binding protein)
Fields
>>Salivary secretion
Human protein sequence Database
Q9UGM3
Mouse protein sequence database
Q60997
Rat protein sequence database
Q8CIZ5
Cellular localization
Secreted . Some isoforms may be membrane-bound. Localized to the lumenal aspect of crypt cells in the small intestine. In the colon, seen in the lumenal aspect of surface epithelial cells. Formed in the ducts of von Ebner gland, and released into the fluid bathing the taste buds contained in the taste papillae (By similarity). .
Tissue expression
Highly expressed in alveolar and macrophage tissues. In some macrophages, expression is seen on the membrane, and in other macrophages, strongly expressed in the phagosome/phagolysosome compartments. Expressed in lung, trachea, salivary gland, small intestine and stomach. In pancreas, expressed in certain cells of the islets of Langerhans. In digestive tract, confined to tissues with large epithelial surfaces. In intestinal tissue, moderately expressed in epithelial cells of the midcrypts and the crypt base. Expression is significantly elevated in intestinal tissue from patients with inflammatory bowel disease (IBD), particularly in surface epithelial and Paneth cells, but not in IBD patients with mutant NOD2. Present in crypt bases of the duodenum, in crypt tops of the colon, and in colle
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