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  • 1
    Publication Date: 2002-03-02
    Description: The gastrointestinal tract is lined by a layer of mucus comprised of highly glycosylated proteins called mucins. To evaluate the importance of mucin in intestinal carcinogenesis, we constructed mice genetically deficient in Muc2, the most abundant secreted gastrointestinal mucin. Muc2-/- mice displayed aberrant intestinal crypt morphology and altered cell maturation and migration. Most notably, the mice frequently developed adenomas in the small intestine that progressed to invasive adenocarcinoma, as well as rectal tumors. Thus, Muc2 is involved in the suppression of colorectal cancer.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Velcich, Anna -- Yang, WanCai -- Heyer, Joerg -- Fragale, Alessandra -- Nicholas, Courtney -- Viani, Stephanie -- Kucherlapati, Raju -- Lipkin, Martin -- Yang, Kan -- Augenlicht, Leonard -- CA 72835/CA/NCI NIH HHS/ -- CA 90808/CA/NCI NIH HHS/ -- P0 CA 13330/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2002 Mar 1;295(5560):1726-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Oncology, Albert Einstein Cancer Center/Montefiore Medical Center, 111 East 210 Street, Bronx, NY 10467, USA. velcich@aecom.yu.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11872843" target="_blank"〉PubMed〈/a〉
    Keywords: Adenocarcinoma/chemistry/pathology ; Adenoma/chemistry/pathology ; Animals ; Apoptosis ; Cell Differentiation ; Cell Division ; Cell Lineage ; Cell Movement ; Colon/chemistry/cytology/pathology ; Colorectal Neoplasms/*etiology/metabolism/pathology ; Cytoskeletal Proteins/analysis ; Disease Progression ; Duodenal Neoplasms/chemistry/pathology ; Duodenum/chemistry/cytology/pathology ; Epithelial Cells/chemistry/physiology ; Female ; Gene Targeting ; Goblet Cells/cytology ; Intestinal Mucosa/chemistry/cytology/pathology ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Mutant Strains ; Mucin-2 ; Mucins/analysis/*genetics/*physiology ; Proto-Oncogene Proteins c-myc/analysis ; *Trans-Activators ; beta Catenin
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 2
    Publication Date: 2009-05-30
    Description: Intracellular trafficking of the glucose transporter GLUT4 from storage compartments to the plasma membrane is triggered in muscle and fat during the body's response to insulin. Clathrin is involved in intracellular trafficking, and in humans, the clathrin heavy-chain isoform CHC22 is highly expressed in skeletal muscle. We found a role for CHC22 in the formation of insulin-responsive GLUT4 compartments in human muscle and adipocytes. CHC22 also associated with expanded GLUT4 compartments in muscle from type 2 diabetic patients. Tissue-specific introduction of CHC22 in mice, which have only a pseudogene for this protein, caused aberrant localization of GLUT4 transport pathway components in their muscle, as well as features of diabetes. Thus, CHC22-dependent membrane trafficking constitutes a species-restricted pathway in human muscle and fat with potential implications for type 2 diabetes.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2975026/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2975026/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vassilopoulos, Stephane -- Esk, Christopher -- Hoshino, Sachiko -- Funke, Birgit H -- Chen, Chih-Ying -- Plocik, Alex M -- Wright, Woodring E -- Kucherlapati, Raju -- Brodsky, Frances M -- GM038093/GM/NIGMS NIH HHS/ -- HD47863/HD/NICHD NIH HHS/ -- R01 GM038093/GM/NIGMS NIH HHS/ -- R01 GM038093-19/GM/NIGMS NIH HHS/ -- R01 GM038093-19S1/GM/NIGMS NIH HHS/ -- R01 GM038093-20A1/GM/NIGMS NIH HHS/ -- R01 HD047863/HD/NICHD NIH HHS/ -- R01 HD047863-01/HD/NICHD NIH HHS/ -- R01 HD047863-02/HD/NICHD NIH HHS/ -- R01 HD047863-03/HD/NICHD NIH HHS/ -- R01 HD047863-04/HD/NICHD NIH HHS/ -- R01 HD047863-05/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 2009 May 29;324(5931):1192-6. doi: 10.1126/science.1171529.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Bioengineering and Therapeutic Sciences, University of California, School of Pharmacy, San Francisco (UCSF), San Francisco, CA 94143, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19478182" target="_blank"〉PubMed〈/a〉
    Keywords: Adipocytes/cytology/*metabolism/ultrastructure ; Animals ; Blood Glucose/metabolism ; Cell Differentiation ; Cell Line ; Cell Membrane/metabolism ; Clathrin/chemistry/*metabolism ; Clathrin Heavy Chains ; Clathrin-Coated Vesicles/*metabolism ; Diabetes Mellitus, Type 2/*metabolism ; Glucose/*metabolism ; Glucose Transporter Type 4/*metabolism ; Humans ; Insulin/blood/pharmacology ; Mice ; Mice, Transgenic ; Muscle Fibers, Skeletal/metabolism ; Muscle, Skeletal/*metabolism/ultrastructure ; Myoblasts/cytology/metabolism/ultrastructure ; Protein Isoforms/chemistry/metabolism ; Protein Transport ; Signal Transduction
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
    Publication Date: 1983-07-08
    Description: A diffusible factor produced and secreted by malignant murine cells was capable of inducing plasminogen activator production by normal diploid human fibroblasts. The factor's ability to induce plasminogen activator was insensitive to treatment with nucleases, but its activity was destroyed by digestion with proteases. It is proposed that such a factor would play a role in malignancy if it would recruit normal cells that were adjacent to transformed cells to produce plasminogen activator which could result in tumor-promoted proteolysis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Davies, R L -- Rifkin, D B -- Tepper, R -- Miller, A -- Kucherlapati, R -- CA-16239/CA/NCI NIH HHS/ -- CA-35171/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1983 Jul 8;221(4606):171-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6682999" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cricetinae ; Fibroblasts/drug effects/metabolism ; Humans ; Hybrid Cells/metabolism ; Melanoma/metabolism ; Mice ; Neoplasms, Experimental/*metabolism/secretion ; Peptides/pharmacology/*secretion ; Plasminogen Activators/*biosynthesis ; Rats
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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