DNAprint Genomics (DNAG)

[johnnyfiber]

I suspect there are a number of diagnostic/theranostic tests DnaPrint will develop asociated with cd-59. Type II diabetes, cardiovascular...will also have oncological applications:

2007 Jan 26

Small-Molecule Inhibition of the Interaction between the Translation Initiation Factors eIF4E and eIF4G.

[My paper] Nathan J Moerke , Huseyin Aktas , Han Chen , Sonia Cantel , Mikhail Y Reibarkh , Amr Fahmy , John D Gross , Alexei Degterev , Junying Yuan , Michael Chorev , Jose A Halperin , Gerhard Wagner

Assembly of the eIF4E/eIF4G complex has a central role in the regulation of gene expression at the level of translation initiation. This complex is regulated by the 4E-BPs, which compete with eIF4G for binding to eIF4E and which have tumor-suppressor activity. To pharmacologically mimic 4E-BP function we developed a high-throughput screening assay for identifying small-molecule inhibitors of the eIF4E/eIF4G interaction. The most potent compound identified, 4EGI-1, binds eIF4E, disrupts eIF4E/eIF4G association, and inhibits cap-dependent translation but not initiation factor-independent translation. While 4EGI-1 displaces eIF4G from eIF4E, it effectively enhances 4E-BP1 association both in vitro and in cells. 4EGI-1 inhibits cellular expression of oncogenic proteins encoded by weak mRNAs, exhibits activity against multiple cancer cell lines, and appears to have a preferential effect on transformed versus nontransformed cells. The identification of this compound provides a new tool for studying translational control and establishes a possible new strategy for cancer therapy.

http://209.85.165.104/search?q=cache:tq4JpGcCzFMJ:lib.bioinfo.pl/auth:Chorev,M+Dr.+Michael+Chorev+20....

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Inhibitor of CD59 Activity as an Adjunct to Antibody-Based Cancer Therapy

http://otd.harvard.edu/technologies/tech.php?case=2887

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Abstract: Type 2 diabetes mellitus (T2DM) can lead to death without treatment and it has been predicted that the condition will affect 215 million people worldwide by 2010. T2DM is a multifactorial disorder whose precise genetic causes and biochemical defects have not been fully elucidated, but at both levels, calpains appear to play a role. Positional cloning studies mapped T2DM susceptibility to CAPN10, the gene encoding the intracellular cysteine protease, calpain 10. Further studies have shown a number of noncoding polymorphisms in CAPN10 to be functionally associated with T2DM while the identification of coding polymorphisms, suggested that mutant calpain 10 proteins may also contribute to the disease. Here we review recent studies, which in addition to the latter enzyme, have linked calpain 5, calpain 3, and its splice variants, calpain 2 and calpain 1 to T2DM-related metabolic pathways along with T2DM-associated phenotypes, such as obesity and impaired insulin secretion, and T2DM-related complications, such as epithelial dysfunction and diabetic cataract.

http://www.blackwell-synergy.com/doi/abs/10.1196/annals.1372.011?journalCode=nyas

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Calpain-5 gene variants are associated with diastolic blood pressure and cholesterol levels

1Departamento de Genómica Estructural. Neocodex. Sevilla, Spain

Genes implicated in common complex disorders such as obesity, type 2 diabetes mellitus (T2DM) or cardiovascular diseases are not disease specific, since clinically related disorders also share genetic components. Cysteine protease Calpain 10 (CAPN10) has been associated with T2DM, hypertension, hypercholesterolemia, increased body mass index (BMI) and polycystic ovary syndrome (PCOS), a reproductive disorder of women in which isunlin resistance seems to play a pathogenic role. The calpain 5 gene (CAPN5) encodes a protein homologue of CAPN10. CAPN5 has been previously associated with PCOS by our group. In this new study, we have analysed the association of four CAPN5 gene variants(rs948976A>G, rs4945140G>A, rs2233546C>T and rs2233549G>A) with several cardiovascular risk factors related to metabolic syndrome in general population

http://www.biomedcentral.com/1471-2350/8/1#B41

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DNAPRINT GENOMICS ANNOUNCES STRATEGIC ALLIANCE WITH NEOCODEX

http://www.dnaprint.com/welcome/press/press_recent/2006/0822/DNAG-NEOCODEX.pdf

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Genetic Markers
Progress and Potential for Cardiovascular Disease

By tracking the progression of heart failure from the initial event (eg, cardiomyopathy) to end-stage failure using genomic techniques, researchers can develop a better understanding of the molecular processes involved. Using this approach, we have proposed more than a dozen biomarkers of dilated cardiomyopathy (ANP, lumican, ITP 3-kinase, etc), hypertrophic cardiomyopathy (CD59, HSP90, calpain, etc), and end-stage heart failure (desmin, dynamitin, nucleolin, etc), respectively.138,141,145 This combined approach has also been successfully used in animal models of hypertension and has significant implications for the study of human disease.147


http://circ.ahajournals.org/cgi/content/full/109/25_suppl_1/IV-47

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Harvard University Receives Notice of Allowance on Diagnostic Patent Claims Licensed to DNAPrint Genomics, Inc.

SARASOTA, FL -- (MARKET WIRE) -- March 09, 2006 -- DNAPrint Genomics, Inc. (OTC BB: DNAG) today announced that Harvard University has received formal Notice of Allowance from the U.S. Patent and Trademark Office (USPTO) for 20 claims that cover diagnostic uses of a novel marker for diabetes licensed by the Company. DNAPrint entered into an agreement with Harvard in January 2006 to sponsor continued research based on the marker, CD59, in the Harvard Medical School laboratory of Dr. Jose Halperin, a named inventor of the allowed claims. These claims, once issued, will provide Harvard additional intellectual property protection to support the development and commercialization by DNAPrint of new diagnostic tests to better define and manage diabetes more effectively.

http://www.marketwire.com/mw/release_html_b1?release_id=112547