Neuronal toxicity of efavirenz: a systematic review.
Stellenbosch, South Africa. In Expert Opin Drug Saf, 30 Nov 2013
Several potential mechanisms exist to explain the observed efavirenz neurotoxicity, including altered calcium hemostasis, decreases in brain creatine kinase, mitochondrial damage, increases in brain proinflammatory cytokines and involvement of the cannabinoid system.
Proteomic analysis of time-dependent changes in proteins expressed in mouse hippocampus during synaptic plasticity induced by GABAA receptor blockade.
Himeji, Japan. In Neurosci Lett, 25 Nov 2013
Expression of 14 proteins (i.e., dihydropyrimidinase-related protein 2, α-tubulin isotype M-α-2, tubulin β-1 chain, tubulin β-2A chain, protein disulfide-isomerase ERp61 precursor, chaperonin-containing T complex polypeptide 1 β subunit, T complex polypeptide 1 [partial], creatine kinase B-type, cytosolic malate dehydrogenase [partial], vacuolar adenosine triphosphatase subunit A, and uncharacterized protein LOC433182) was increased and expression of one protein (i.e., actin γ, cytoplasmic 1) was decreased.
Resistance Artery Creatine Kinase mRNA and Blood Pressure in Humans.
Amsterdam, Netherlands. In Hypertension, 14 Nov 2013
Normalized creatine kinase B mRNA copy numbers, ranging from 5.2 to 24.4 (mean, 15.0; SE, 1.9), showed a near-perfect correlation with diastolic blood pressure (correlation coefficient, 0.9; 95% confidence interval, 0.6-1.0)
Sequence homology and structure predictions of the creatine kinase isoenzymes.
Zürich, Switzerland. In Mol Cell Biochem, 1994
A 'CK framework' is defined, consisting of the most conserved sequence blocks, and 'diagnostic boxes' are identified which are characteristic for anyone creatine kinase isoenzyme (e.g. for vertebrate B-CK) and which may serve to distinguish this isoenzyme from all others (e.g. from M-CKs and Mi-CKs).