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  • 1
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    Basal cell carcinomas in mice overexpressing sonic hedgehog (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-05-02
    Description: Mutations in the tumor suppressor gene PATCHED (PTC) are found in human patients with the basal cell nevus syndrome, a disease causing developmental defects and tumors, including basal cell carcinomas. Gene regulatory relationships defined in the fruit fly Drosophila suggest that overproduction of Sonic hedgehog (SHH), the ligand for PTC, will mimic loss of ptc function. It is shown here that transgenic mice overexpressing SHH in the skin develop many features of basal cell nevus syndrome, demonstrating that SHH is sufficient to induce basal cell carcinomas in mice. These data suggest that SHH may have a role in human tumorigenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Oro, A E -- Higgins, K M -- Hu, Z -- Bonifas, J M -- Epstein, E H Jr -- Scott, M P -- AR39959/AR/NIAMS NIH HHS/ -- New York, N.Y. -- Science. 1997 May 2;276(5313):817-21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Dermatology, Stanford University School of Medicine, Stanford, CA 94305-5427, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9115210" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Basal Cell Nevus Syndrome/*genetics/metabolism/pathology ; Carcinoma, Basal Cell/*genetics/metabolism/pathology ; Embryo, Mammalian ; *Gene Expression Regulation, Neoplastic ; Hedgehog Proteins ; Humans ; Intracellular Signaling Peptides and Proteins ; Keratinocytes/metabolism ; Male ; Membrane Proteins/genetics/metabolism ; Mice ; Mice, SCID ; Mice, Transgenic ; Mutation ; Neoplasm Transplantation ; Protein Biosynthesis ; Proteins/*genetics/metabolism ; Receptors, Cell Surface ; Skin/pathology ; Skin Neoplasms/*genetics/metabolism/pathology ; Skin Transplantation ; *Trans-Activators
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 2
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    GLI activation by atypical protein kinase C iota/lambda regulates the growth of basal cell carcinomas (2013)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2013-03-01
    Description: Growth of basal cell carcinomas (BCCs) requires high levels of hedgehog (HH) signalling through the transcription factor GLI. Although inhibitors of membrane protein smoothened (SMO) effectively suppress HH signalling, early tumour resistance illustrates the need for additional downstream targets for therapy. Here we identify atypical protein kinase C iota/lambda (aPKC-iota/lambda) as a novel GLI regulator in mammals. aPKC-iota/lambda and its polarity signalling partners co-localize at the centrosome and form a complex with missing-in-metastasis (MIM), a scaffolding protein that potentiates HH signalling. Genetic or pharmacological loss of aPKC-iota/lambda function blocks HH signalling and proliferation of BCC cells. Prkci is a HH target gene that forms a positive feedback loop with GLI and exists at increased levels in BCCs. Genome-wide transcriptional profiling shows that aPKC-iota/lambda and SMO control the expression of similar genes in tumour cells. aPKC-iota/lambda functions downstream of SMO to phosphorylate and activate GLI1, resulting in maximal DNA binding and transcriptional activation. Activated aPKC-iota/lambda is upregulated in SMO-inhibitor-resistant tumours and targeting aPKC-iota/lambda suppresses signalling and growth of resistant BCC cell lines. These results demonstrate that aPKC-iota/lambda is critical for HH-dependent processes and implicates aPKC-iota/lambda as a new, tumour-selective therapeutic target for the treatment of SMO-inhibitor-resistant cancers.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3761364/" 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/PMC3761364/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Atwood, Scott X -- Li, Mischa -- Lee, Alex -- Tang, Jean Y -- Oro, Anthony E -- 1F32CA14208701/CA/NCI NIH HHS/ -- AR046786/AR/NIAMS NIH HHS/ -- AR052785/AR/NIAMS NIH HHS/ -- R01 AR046786/AR/NIAMS NIH HHS/ -- R01 AR052785/AR/NIAMS NIH HHS/ -- R01 AR054780/AR/NIAMS NIH HHS/ -- England -- Nature. 2013 Feb 28;494(7438):484-8. doi: 10.1038/nature11889.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Program in Epithelial Biology, Stanford University School of Medicine, Stanford, California 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23446420" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Carcinoma, Basal Cell/drug therapy/enzymology/*metabolism/*pathology ; Cell Line, Tumor ; Cell Proliferation/drug effects ; Cells, Cultured ; Centrosome/metabolism ; Drug Resistance, Neoplasm ; Feedback, Physiological ; Hedgehog Proteins/metabolism ; Humans ; Isoenzymes/antagonists & inhibitors/genetics/*metabolism ; Keratinocytes/metabolism ; Kruppel-Like Transcription Factors/genetics/*metabolism ; Mice ; Phosphorylation ; Protein Kinase C/antagonists & inhibitors/genetics/*metabolism ; Receptors, G-Protein-Coupled/antagonists & inhibitors/metabolism ; Signal Transduction/drug effects ; Transcription Factors/*metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 3
    Electronic Resource
    Electronic Resource
    Molecular analysis of the inheritance and stability of the mitochondrial genome of an inbred line of maize (1985)
    Springer
    Theoretical and applied genetics 70 (1985), S. 287-293 
    Details
    ISSN: 1432-2242
    Keywords: Mitochondrial DNA ; Maize ; Restriction endonuclease digestion patterns
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Summary We have investigated the inheritance of the mitochondrial DNA (mtDNA) restriction endonuclease digestion patterns of maize inbred line B37N in individual plants and pooled siblings in lineages derived from five separate plants in the third generation following successive self-pollinations. The restriction fragment patterns of the different mtDNA samples were compared after digestion with five endonucleases. No differences were visible in the mobilities of the 199 fragments scored per sample. Hybridization analysis with two different cloned mtDNA probes, one of which contains homologies to a portion of the S2 plasmid characteristic of cms-S maize, failed to reveal cryptic variation. The apparent rate of genomic change in maize mtDNA from inbred plants appears to be very slow, compared with the faster rates of change seen in maize tissue cultures and with the documented rapid rate of inter- and intraspecific variation for mammalian mtDNA.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00304913
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  • 4
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    Bone morphogenetic protein antagonist gremlin 1 is widely expressed by cancer-associated stromal cells and can promote tumor cell proliferation (2006)
    National Academy of Sciences
    Details
    Publication Date: 2006-09-26
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
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