Nature, 456, 745-749, 2008
Gordon GR, Choi HB, Rungta RL, Ellis-Davies GC, & Macvicar BA
Brain metabolism dictates the polarity of astrocyte control over arterioles
This excellent work demonstrates a metabolic coupling of cerebral blood to the lactate/pyruvate ratio and the related NADH/NAD ratio. The authors tested the hypothesis that the metabolic
state of the tissue dictates the type of astrocyte influence on arteriole diameter, and were able to reliably measure extracellular lactate levels using our L-Lactate Assay Kit (cat#: A-108S and
A-108L). Please note that a D-Lactate Assay Kit has recently become available. Additional citations of our L-Lactate Assay Kit are listed below.
J Pharmacol Exp Ther, 333:341-50, 2010
PLoS One, 5:e13820, 2010
Am J Physiol, 294:E148-E156, 2008
J Biol Chem, 282:1607-14, 2007
J Bacteriol, 189:8079-87, 2007
J Biol Chem, 281:26769-26773, 2006
PLOS ONE 10(3): e0121046, 2015
Chung-Ling Lu, Lili Qin, Hsin-Chen Liu, Demet Candas, Ming Fan, Jian Jian Li
Tumor Cells Switch to Mitochondrial Oxidative Phosphorylation under Radiation via mTOR-Mediated Hexokinase II Inhibition - A Warburg-Reversing Effect
The study demonstrates that a unique feature of cancer cells is to convert glucose into lactate to produce cellular energy, even under the presence of oxygen. The authors report that mTOR
can be relocated to mitochondria, and as a result, enhances oxidative phosphorylation and reduces glycolysis. The authors measured hexokinase activity using our Hexokinase Assay Kit
(cat#: E-111). Additional citation of our HK Assay Kit is listed below.
Cancer & Metabolism 1:2, 2013
AGE 36:21, 2014
Proc Natl Acad Sci USA, 103, 18751-18756, 2006
Zaki M, Andrew N, & Insall RH
Entamoeba histolytica cell movement: A central role for self-generated chemokines and chemorepellents
This interesting work by Zaki et al sought to understand the mechanism governing motility of E. histolytica, the cause of amoebic dysentery, within the G.I. tract. They discovered that
components of E. histolytica-conditioned culture medium are key determinants of cell motility. Using our Ethanol Assay Kit (cat#: A-111), the authors were able to confirm that the
chemokinetic but not the chemotactic effect of conditioned medium could be completely recreated by physiological ethanol levels. Related assay kits offered by us include Alcohol
Dehydrogenase Assay Kit and Aldehyde Dehydrogenase Assay Kit. Additional citations of our Ethanol Assay kit are listed below.
J Pharmacol Exp Therapy 346:504-513,2013
Alcoholism, 34:997-1005, 2010
J Biol Chem, 286:99-113, 2011
Giulivi C, Ross-Inta C, Omanska-Klusek A, Napoli E, Sakaguchi D, Barrientos G, Allen PD, & Pessah IN
Basal bioenergetic abnormalities in skeletal muscle from ryanodine receptor malignant hyperthermia-susceptible R163C knock-in mice
Malignant hyperthermia (MH), a genetic disorder of skeletal muscle associated with mutations in the ryanodine receptor (RyR1), is characterized by an abnormal response to muscle
depolarizing muscle relaxants. This insightful study focused metabolic differences in MH susceptible and normal skeletal muscle under basal conditions using C57BL6 WT mice and C57BL6
knock-in mice expressing the R163CRyR1 mutation, which is one of the most common human MH mutations. Using our Glyceraldehyde-3-Phosphate (GAPDH) Dehydrogenase Assay Kit
(cat#: E-101), they were able to demonstrate that these changes are associated with lower GAPDH expression and activity. Additional citations of our GAPDH Assay kit are listed below.
Gynecol Oncol, 107:450-457, 2007
Mol Cell Biochem, 321:45-52, 2009
J Orthopedic Res, 28:914-920, 2010
Cancer Res, 66:1684-1693, 2006
Dang DT, Chen F, Gardner LB, Cummins JM, Rago C, Bunz F, Kantsevoy SV, & Dang LH
Hypoxia-inducible factor-1α promotes nonhypoxia-mediated proliferation in colon cancer cells and xenografts
The hypoxia-inducible transcription factor HIF-1α is strongly associated with cancer cell growth and survival. In this article, the authors disrupted HIF-1α by targeted homologous recombination
in HCT116 and RKO human colon cancer cells, and elegantly show that HIF-1α promotes nonhypoxia-mediated cell proliferation in vitro and in vivo in a subset of colon cancers. Using our ATP
Assay Kit (cat#: A-107), they measured levels of ATP and other metabolites in glycolysis under normoxic culture conditions. We also have ATP/ADP/AMP Assay Kit (cat#:A-125). Additional
citations of our ATP Assay Kit are listed below.
Mol Cancer, 9:293-304, 2010
J Ethnopharmacol, 130: 614-620, 2010
Eur J Pharmacol, 627: 85-91, 2010
J Mol Cell Cardiol, 45:385-393, 2008
Chiu J, Farhangkhoee H, Xu BY, Chen S, George B, & Chakrabarti S
PARP mediates structural alterations in diabetic cardiomyopathy
Diabetic cardiomyopathy is a unique disease that directly affects the structure and the function of the myocardium in the absence of coronary artery disease or hypertension. The authors
investigated the role of PARP in the development of structural changes in the diabetic heart, and determined whether these changes might be mediated by p300, a histone acetyltransferase.
Using our Catalase Assay Kit (cat#: E-100), the authors demonstrated that hyperglycemia caused upregulation of extracellular matrix proteins and p300 and increased oxidative stress.
Related assay kits offered by us include Peroxide Assay and Lipid Peroxidation Assay Kits. Additional citations of our Catalase Assay Kit are listed below.
PLoS One, 5:e12427, 2010
Cancer Res, 69: 5560-5567, 2009
AGE 36:21, 2014
Scientific Reports 6:22788, 2016
Cancer Res, 69:5560-5567, 2009
Lynch J, Fukuda Y, Krishnamurthy P, Du G, & Schuetz JD
Cell survival under stress is enhanced by a mitochondrial ATP-binding cassette transporter that regulates hemoproteins
The ATP-binding cassette (ABC) transporter ABCB6 gene is amplified in camptothecin-resistant cells, and its overexpression is associated with multiagent resistance. The authors showed that
increased ABCB6 expression alters the levels of cellular hemoproteins and provides a cell survival advantage. Using our Lactate Dehydrogenase (LDH) Assay Kit (cat#: E-107) to determine
the activity of cytosolic LDH, they showed that increased heme in ABCB6-expressing cells did not alter the expression of either mitochondrial or cytosolic proteins. Additional citations of our
LDH Assay kit are listed below.
Cancer Res, 66:1684-1693, 2006
J Anim Sci, 87:3124-3133, 2009
Mol Therapy 2:e136,2013
ANTIOXIDANTS & REDOX SIGNALING, 12:819-827, 2010
Yoo MH, Gu X, Xu XM, Kim JY, Carlson BA, Patterson AD, Cai H, Gladyshev VN, Hatfield DL
Delineating the Role of Glutathione Peroxidase 4 in Protecting Cells Against Lipid Hydroperoxide Damage and in Alzheimer’s Disease
The authors characterized the function of glutathione peroxidase 4 (GPx4) by targeting GPx4 downregulation using RNA interference. Partial knockdown of GPx4 levels resulted in growth
retardation and morphological changes. Using our Lipid Peroxidation (MDA) Assay Kit, they analyzed brain tissues of mice suffering from a model of Alzheimer’s disease and found that
oxidized lipid by-products were enriched, and expression of GPx4 was downregulated. Additional citation of our Lipid Peroxidation Assay Kit is listed below.
Neuron 82, 195–207, April 2, 2014
Transplantation 87:1275, 2009
Mol Cell Biochem 321:45, 2009
Biochemical Journal, 433:51-63, 2011
AGGARWAL S, SUZUKI T, TAYLOR WL, BHARGAVA A, and RAO RK
Contrasting effects of ERK on tight junction integrity in differentiated and under-differentiated Caco-2 cell monolayers
The authors investigated the effect of the state of cell differentiation on ERK-mediated regulation of tight junctions in Caco-2 cell monolayers. Using our ALP Assay Kit, they found that EGF
(epidermal growth factor) potentiated H2O2-induced tight junction disruption in under-differentiated cell monolayers. The study concludes that ERK may exhibit its contrasting influences on
tight junction integrity in underdifferentiated and differentiated epithelial cells by virtue of differences in its subcellular distribution and ability to regulate the association of PKCζ and PP2A with
tight junction proteins. Additional citation of our ALP Assay Kit is listed below.
Cell Transplantation 17:911, 2008
J Cell Physiology 216:458, 2008
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