D
David L. Vander Jagt
Researcher at University of New Mexico
Publications - 100
Citations - 6188
David L. Vander Jagt is an academic researcher from University of New Mexico. The author has contributed to research in topics: Aldose reductase & Methylglyoxal. The author has an hindex of 40, co-authored 100 publications receiving 5804 citations. Previous affiliations of David L. Vander Jagt include Rutgers University.
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Inhibition of lactate dehydrogenase A induces oxidative stress and inhibits tumor progression
Anne Le,Charles R. Cooper,Arvin M. Gouw,Ramani Dinavahi,Anirban Maitra,Lorraine M. Deck,Robert E. Royer,David L. Vander Jagt,Gregg L. Semenza,Chi V. Dang +9 more
TL;DR: It is shown that inhibition of LDHA with FX11 is an achievable and tolerable treatment for LDHA-dependent tumors and oxidative stress and cell death are critical aspects of cancer biology to consider for the therapeutical targeting of cancer energy metabolism.
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Purification of glutathione S-transferases from human liver by glutathione-affinity chromatography.
TL;DR: Multiple forms of glutathione S -transferase, a family of proteins involved both with bilirubin transport and with the detoxification of electrophiles, have been purified from human liver using a scheme which employs an affinity chromatography column prepared by coupling glutathion to epoxy-activated Sepharose.
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Anti-oxidant activities of curcumin and related enones.
TL;DR: The natural product curcumin, obtained from the spice turmeric, exhibits numerous biological activities including anti-cancer, anti-inflammatory, and anti-angiogenesis activities; some of these biological activities may derive from its anti-oxidant properties.
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Methylglyoxal metabolism and diabetic complications: roles of aldose reductase, glyoxalase-I, betaine aldehyde dehydrogenase and 2-oxoaldehyde dehydrogenase.
TL;DR: The 2-oxoaldehyde methylglyoxal (MeG) is the precursor to a number of the known advanced glycation endproducts (AGE) implicated in the development of diabetic complications, and rates of production of MeG depend upon physiological conditions such as hyperglycemia and ketoacidosis.
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Homocysteine Increases the Expression of Vascular Endothelial Growth Factor by a Mechanism Involving Endoplasmic Reticulum Stress and Transcription Factor ATF4
C. Nathaniel Roybal,Shujie Yang,Chiao-Wang Sun,Diego Hurtado,David L. Vander Jagt,Tim M. Townes,Steve F. Abcouwer +6 more
TL;DR: These studies indicate that expression of the pro-angiogenic factor VEGF is increased by homocysteine and other thiol-containing reductive compounds via ATF4-dependent activation of V EGF transcription.