"Amplification and expression of the c-myc oncogene in human lung cancer cell lines
NCI-Navy Medical Oncology Branch, National Cancer Institute, National Institutes of Health, and Naval Hospital, Bethesda, Maryland 20814, USA
Genetic changes involving the c-myc oncogene have been observed in human tumours. In particular, the c-myc gene is translocated in Burkitt's lymphoma1–3 and is amplified in the human promyelocytic leukaemia cell line...."
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(If you happen not to find a target for therapy, call CRBCM, immediately!) today VITAMIN D is given at 50,000 IU weekly.
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Calcitriol acts through its receptor, the Calcitriol receptor of course, will eventually interact with a Zinc finger and BTB domain-containing protein 16, encoded by the ZBTB16, a popular gene that will engage events in the epigenetic areas which include many receptors (watch out because even the Angiotensin receptor is engaged). But ultimately the RUNX and the GATA2 are also engaged. The involvement of SN3A and MDX1 however will have the most importance when it comes to c-MYC since these gene impact the Mad-Max complex. And you know what c-MYC needs to be active (association with MAX),
let Wikipedia tell you:
MXD1
From Wikipedia, the free encyclopedia
MAX dimerization protein 1 | |||||||||||
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PDB rendering based on 1nlw. |
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Identifiers | |||||||||||
Symbols | MXD1; BHLHC58; MAD; MAD1 | ||||||||||
External IDs | OMIM: 600021 MGI: 96908 HomoloGene: 1767 GeneCards: MXD1 Gene | ||||||||||
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RNA expression pattern | |||||||||||
More reference expression data | |||||||||||
Orthologs | |||||||||||
Species | Human | Mouse | |||||||||
Entrez | 4084 | 17119 | |||||||||
Ensembl | ENSG00000059728 | ENSMUSG00000001156 | |||||||||
UniProt | Q05195 | Q8K1Z8 | |||||||||
RefSeq (mRNA) | NM_001202513 | NM_010751 | |||||||||
RefSeq (protein) | NP_001189442 | NP_034881 | |||||||||
Location (UCSC) | Chr 2: 70.12 – 70.17 Mb |
Chr 6: 86.65 – 86.67 Mb |
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PubMed search | [1] | [2] | |||||||||
MAD-MAX dimerization protein belongs to a subfamily of MAX-interacting proteins. This protein competes with MYC for binding to MAX to form a sequence-specific DNA-binding complex, acts as a transcriptional repressor (while MYC appears to function as an activator) and is a candidate tumor suppressor.[2] The MAD-MAX protein dimer may be a reference to the popular cult classic film Mad Max (1979)."wikipedia
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FOR A CAREFUL PREVENTION PROGRAM USING VITAMIN D, OR ASSOCIATION OF VITAMIN D IN TREATMENTS OF MENTIONED CANCERS, LET'S WORK HARD! (whenever focusing on c-MYC, don't forget the FUSE or FUBP1)
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