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    Keywords: brain ; RECEPTOR ; CELLS ; EXPRESSION ; tumor ; CELL ; Germany ; human ; LUNG ; liver ; SITE ; PROTEIN ; RNA ; TISSUE ; TUMORS ; TISSUES ; BINDING ; MEMBER ; SEQUENCE ; antibodies ; antibody ; GLYCOPROTEIN ; MOUSE ; Western-blot ; SUPERFAMILY ; innate immunity ; EPITHELIAL-CELLS ; TRACT ; INTERACTS ; TESTIS ; GASTROINTESTINAL-TRACT ; western blot ; salivary gland ; TERMINAL DIFFERENTIATION ; BINDS ; C-type lectin ; collectin ; DENMARK ; DMBT1 ; GP-340 ; HENSIN ; MUCOSA ; PANCREATIC ACINAR-CELLS ; SALIVARY AGGLUTININ ; scavenger receptors ; SURFACTANT PROTEIN-D ; ZYMOGEN GRANULES
    Abstract: CRP-ductin is a protein expressed mainly by mucosal epithelial cells in the mouse. Sequence homologies indicate that CRP-ductin is the mouse homologue of human gp-340, a glycoprotein that agglutinates microorganisms and binds the lung mucosal collectin surfactant protein-D (SP-D). Here we report that purified CRP-ductin binds human SP-D in a calcium-dependent manner and that the binding is not inhibited by maltose. The same properties have previously been observed for gp-340 binding of SP-D. CRP-ductin also showed calcium-dependent binding to both gram-positive and -negative bacteria. A polyclonal antibody raised against gp-340 reacted specifically with CRP-ductin in Western blots. Immunoreactivity to CRP-ductin was found in the exocrine pancreas, in epithelial cells throughout the gastrointestinal tract and in the parotid ducts. A panel of RNA preparations from mouse tissues was screened for CRP-ductin and SP-D expression by reverse transcription-PCR. The pancreas was the main site of synthesis of CRP-ductin, but transcripts were also readily amplified from salivary gland, the gastrointestinal tract, liver, testis, uterus and lung. Lung was the main site of synthesis of SP-D, but transcripts were also amplified from uterus, salivary gland, thymus, thyroid gland, pancreas and testis. We conclude that CRP-ductin is the mouse homologue of human gp-340 and that its capacity to bind SP-D as well as gram-negative and gram-positive bacteria suggests a role in mucosal immune defense
    Type of Publication: Journal article published
    PubMed ID: 12884308
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    Keywords: brain ; RECEPTOR ; CELLS ; EXPRESSION ; tumor ; CELL ; Germany ; IN-VIVO ; VIVO ; DISEASE ; RISK ; GENOME ; HYBRIDIZATION ; PROTEIN ; SAMPLE ; TISSUE ; TUMORS ; MICE ; PATIENT ; DOMAIN ; GENETIC POLYMORPHISMS ; TISSUES ; polymorphism ; POLYMORPHISMS ; SUSCEPTIBILITY ; DELETION ; IN-SITU ; prevention ; immunohistochemistry ; UP-REGULATION ; NUMBER ; PATHOGENESIS ; DISPLAY ; HUMAN GENOME ; SURFACE ; EPITHELIAL-CELLS ; genetic polymorphism ; NORMAL TISSUE ; CHAIN-REACTION ; SMALL-INTESTINE ; ULCERATIVE-COLITIS ; TERMINAL DIFFERENTIATION ; inflammation ; SALIVARY AGGLUTININ ; SURFACTANT PROTEIN-D ; INFLAMMATORY-BOWEL-DISEASE ; MALIGNANT BRAIN-TUMORS ; SCAVENGER RECEPTOR ; in situ hybridization ; CHAIN ; BRAIN-TUMORS ; pathogen ; VARIANT ; ALLELE ; inflammatory bowel disease ; LEVEL ; methods ; SUBTYPES ; SULFATE ; USA ; function ; INCREASED RISK ; odds ratio ; in vivo ; case control ; quantitative ; MUCOSAL ; EXONS ; CRP-DUCTIN ; DEXTRAN SULFATE SODIUM
    Abstract: Background & Aims: Impaired mucosal. defense plays an important role in the pathogenesis of Crohn's disease (CD), one of the main subtypes of inflammatory bowel disease (IBD). Deleted in malignant brain tumors 1(DMBT1) is a secreted scavenger receptor cysteine-rich protein with predominant expression in. the intestine and has been proposed to exert possible functions in regenerative processes and pathogen defense. Here, we aimed at analyzing the role of DMBT1 in IBD. Methods: We studied DMBT1 expression in IBD and normal tissues by quantitative reverse transcription-polymerase chain reaction, immunohistochemistry, and mRNA in situ hybridization. Genetic polymorphisms within DMBT1 were analyzed in an Italian IBD case-control sample. Dmbt1(-/-) mice were generated, characterized, and analyzed for their susceptibility to dextran sulfate sodium-induced colitis. Results: DMBT1 levels correlate with disease activity in inflamed IBD tissues. A highly significant fraction of the patients with IBD displayed up-regulation of DMBT1 specifically in the intestinal epithelial surface cells and Paneth cells. A deletion allele of DMBT1 with a reduced: number of scavenger receptor cysteine-rich domain coding exons is associated with an increased risk of CD (P =.00056; odds ratio, 1.75) but not for ulcerative colitis. Dmbt1(-/-) mice display enhanced susceptibility to dextran sulfate sodium-induced colitis and elevated Tnf, Il6, and Nod2 expression levels during inflammation. Conclusions: DMBT1 may play a role in intestinal mucosal protection and prevention of inflammation. Impaired DMBT1 function may contribute to the pathogenesis of CD
    Type of Publication: Journal article published
    PubMed ID: 17983803
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    Keywords: RECEPTOR ; CANCER ; CELLS ; EXPRESSION ; IN-VITRO ; tumor ; SUPPORT ; SYSTEM ; GENE ; PROTEIN ; PROTEINS ; DIFFERENTIATION ; TUMORS ; LINES ; COMPLEX ; COMPLEXES ; DOMAIN ; INDUCTION ; mechanisms ; SKIN ; MUTATION ; HETEROZYGOSITY ; MELANOMA ; CARCINOMA-CELLS ; EXCHANGE ; EPITHELIAL-CELLS ; squamous cell carcinoma ; epidermis ; TERMINAL DIFFERENTIATION ; DMBT1 ; SALIVARY AGGLUTININ ; basal cell carcinoma ; galectin-3 ; MALIGNANT BRAIN-TUMORS
    Abstract: DMBT1 and galectin-3 are potential interacting proteins with presumably complex roles in tumorigenesis. While at present a variety of mechanisms are discussed for DMBT1 and its participation in cancer, galectin-3 is commonly known to exert tumor-promoting effects. However, in vitro studies in a rodent system have suggested that DMBT1/galectin-3 interaction in the ECM triggers epithelial differentiation, which would point to tumor-suppressive properties. To improve the understanding of DMBT1/galectin-3 action in cancer, we carried out studies in skin cancer of different origins. Mutational analyses of DMBT1 identified a missense mutation in 1 of 13 melanoma cell lines. It led to an exchange of an evolutionary conserved proline residue for serine and located within the second CUB domain of DMBT1. Immunohistochemical analyses demonstrated absence of DMBT1/galectin-3 expression from melanocytes but induction of DMBT1 expression in 1 of 8 nevi and 1 of 11 melanomas and of galectin-3 expression in 3 of 8 nevi and 4 of 8 melanomas. These data suggest that DMBT1 and galectin-3 are unlikely to act as classical tumor suppressors in melanomas. DMBT1 and galectin-3 appear to be secreted to the ECM by epithelial cells within the epidermis and the hair follicle. Compared to the flanking normal epidermis, skin tumors of epithelial origin frequently displayed downregulation of DMBT1 (18 of 19 cases) and galectin-3 (12 of 12 cases). Thus, loss of DMBT1/ galectin- 3 expression may play a role in the genesis of epithelial skin cancer. This would support the view that galectin-3 can exert tumor-suppressive effects in certain scenarios, and DMBT1/galectin-3-mediated differentiation represents a candidate mechanism for this effect. (C) 2003 Wiley-Liss, Inc
    Type of Publication: Journal article published
    PubMed ID: 12673672
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    Keywords: APOPTOSIS ; CELLS ; EXPRESSION ; GROWTH ; tumor ; TOOL ; DISEASE ; GENE ; HYBRIDIZATION ; DIFFERENTIATION ; PATIENT ; SKIN ; T-CELL ; chromosome ; DELETION ; IN-SITU ; LESIONS ; PROGRESSION ; LYMPHOMA ; MUTATION ; ABERRATIONS ; DELETIONS ; LYMPHOCYTES ; FISH ; REGION ; CAENORHABDITIS-ELEGANS ; PHENOTYPE ; ABNORMALITIES ; INTERLEUKIN-2 ; FINLAND ; MYCOSIS-FUNGOIDES ; in situ hybridization ; TUMOR-SUPPRESSOR ; SEZARY-SYNDROME ; allergy ; MISSENSE MUTATION ; SUPPRESSOR ; tumor suppressor gene ; Jurkat cells ; LYMPHOMAS ; CHROMOSOMAL TRANSLOCATIONS ; DISEASE PROGRESSION ; MAMMALIAN HOMOLOG
    Abstract: Multicolor. fluorescent in situ hybridization (FISH) was used to identify acquired chromosomal aberrations in 12 patients with mycosis fungoides or Sezary syndrome, the most common forms of primary cutaneous T-cell lymphoma (CTCL). The most frequently affected chromosome was 12, which showed clonal deletions or translocations with a break point in 12q21 or 12q22 in five of seven consecutive Sezary syndrome patients and a clonal monosomy in the sixth patient. The break point of a balanced translocation t(12;18)(q21;q21.2), mapped in the minimal common region of two deletions, fine mapped to 12q2. By locus-specific FISH, the translocation disrupted one gene, NAV3 (POMFIL1), a human homologue of unc-53 in Caenorhabditis elegans. A missense mutation in the remaining NAV3 allele was found in one of six cases with a deletion or translocation. With locus-specific FISH, NAV3 deletions were found in the skin lesions of four of eight (50%) patients with early mycosis fungoides (stages IA-IIA) and in the skin or lymph node of 11 of 13 (85%) patients with advanced mycosis fungoides or Sezary syndrome. Preliminary functional studies with lentiviral small interfering RNA-based NAV3 silencing in Jurkat cells and in primary lymphocytes showed enhanced interleukin 2 expression (but not CD25 expression). Thus, NAV3 may contribute to the growth, differentiation, and apoptosis of CTCL cells as well as to the skewing from Th1-type to Th2-type phenotype during disease progression. NAV3, a novel putative haploinsufficient tumor suppressor gene, is disrupted in most cases of the commonest types of CTCL and may thus provide a new diagnostic tool
    Type of Publication: Journal article published
    PubMed ID: 16166283
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