Sunday, March 24, 2013

GENES HYPERMETHYLATED TO FAVOR DEDIFFERENTIATION, AND NEOPLASTIC TRANSFORMATION IN LUNG CANCERS

RESEARCHERS SUGGEST THE FOLLOWING GENE AS TARGET FOR HYPERMETHYLATION: 1. DAPK

DAPK1

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Death-associated protein kinase 1

PDB rendering based on 1ig1.
Available structures
PDB Ortholog search: PDBe, RCSB
Identifiers
Symbols DAPK1; DAPK
External IDs OMIM600831 MGI1916885 HomoloGene3626 ChEMBL: 2558 GeneCards: DAPK1 Gene
EC number 2.7.11.1
RNA expression pattern
PBB GE DAPK1 203139 at tn.png
PBB GE DAPK1 211214 s at tn.png
More reference expression data
Orthologs
Species Human Mouse
Entrez 1612 69635
Ensembl ENSG00000196730 ENSMUSG00000021559
UniProt P53355 Q80YE7
RefSeq (mRNA) NM_004938 NM_029653
RefSeq (protein) NP_004929 NP_083929
Location (UCSC) Chr 9:
90.11 – 90.32 Mb
Chr 13:
60.6 – 60.76 Mb

PubMed search [1] [2]
Death-associated protein kinase 1 is an enzyme that in humans is encoded by the DAPK1 gene.[1]
Death-associated protein kinase 1 is a positive mediator of gamma-interferon induced programmed cell death. DAPK1 encodes a structurally unique 160-kD calmodulin dependent serine-threonine kinase that carries 8 ankyrin repeats and 2 putative P-loop consensus sites. It is a tumor suppressor candidate.[2]
In melanocytic cells DAPK1 gene expression may be regulated by MITF.[3]"

AND YOU KNOW THAT ANYONE WHO WANTS TO LIVE WILL SILENCE THIS GENE.  KILLING INTERFERON EFFECT IN LUNG CANCER DESPITE STRESS INDUCTION ROLE IN THE PATHOGENESIS OF LUNG CANCERS.
-------------------------------------------------------------------THIS GENE WAS DISCUSSED IN OTHER BLOG NOTE---------

2. GSTP1

GSTP1

From Wikipedia, the free encyclopedia
Jump to: navigation, search
Glutathione S-transferase pi 1

PDB rendering based on 10gs.
Available structures
PDB Ortholog search: PDBe, RCSB
Identifiers
Symbols GSTP1; DFN7; FAEES3; GST3; GSTP; PI
External IDs OMIM134660 MGI95864 HomoloGene660 ChEMBL: 3902 GeneCards: GSTP1 Gene
EC number 2.5.1.18
RNA expression pattern
PBB GE GSTP1 200824 at tn.png
More reference expression data
Orthologs
Species Human Mouse
Entrez 2950 14869
Ensembl ENSG00000084207 ENSMUSG00000038155
UniProt P09211 P46425
RefSeq (mRNA) NM_000852 NM_181796
RefSeq (protein) NP_000843 NP_861461
Location (UCSC) Chr 11:
67.35 – 67.35 Mb
Chr 19:
4.04 – 4.04 Mb

PubMed search [1] [2]
Glutathione S-transferase P is an enzyme that in humans is encoded by the GSTP1 gene.[1][2]
Glutathione S-transferases (GSTs) are a family of enzymes that play an important role in detoxification by catalyzing the conjugation of many hydrophobic and electrophilic compounds with reduced glutathione. Based on their biochemical, immunologic, and structural properties, the soluble GSTs are categorized into 4 main classes: alpha, mu, pi, and theta. The glutathione S-transferase pi gene (GSTP1) is a polymorphic gene encoding active, functionally different GSTP1 variant proteins that are thought to function in xenobiotic metabolism and play a role in susceptibility to cancer, and other diseases.[3]
GSTP1 has been shown to interact with Fanconi anemia, complementation group C[4][5] and MAPK8.[6]"

METHYLATION HERE IS TO PERPETUATE THE ACTION OF CAUSING FACTORS.  IT IS BAD FOR PATIENTS TO CONTINUE SMOKING ON TREATMENT.  THIS IS AN EARLY EVENT IN TUMOR NEOPLASIA TRANSFORMATION.

Cyclic AMP mediated GSTP1 gene activation in tumor cells involves the interaction of activated CREB-1 with the GSTP1 CRE: a novel mechanism of cellular GSTP1 gene regulation.

PUTING THE EFFECT DEEP INTO THE MITOCHNDRIA.  WHERE THE MTOR INHIBITORS WORK?
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 3.RAR BETA:This gene encodes retinoic acid receptor beta, a member of the thyroid-steroid hormone receptor superfamily of nuclear

transcriptional regulators. This receptor localizes to the cytoplasm and to subnuclear compartments. It binds retinoic
acid, the biologically active form of vitamin A which mediates cellular signalling in embryonic morphogenesis, cell
growth and differentiation. It is thought that this protein limits growth of many cell types by regulating gene
expression. The gene was first identified in a hepatocellular carcinoma where it flanks a hepatitis B virus
integration site. The gene expresses at least two transcript variants; one additional transcript has been described,
but its full length nature has not been determined.
EXPLAINING WHY RETINIOIC ACID (PREVENTION) AND ATRA MAY NOT WORK FULLY!

4.ECAD
5.p14 ARF
6.p16
7.TIMP1
8.FHIT
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