Results 231 to 240 of about 1,205,174 (292)

Mutant p53R273H disrupts PDPK1 homodimerization and contributes to PDPK1 activation

open access: yesMolecular Oncology, EarlyView.
How mutant p53R273H drives AKT signaling is unclear. We show that p53R273H, but not wild‐type, directly binds PDPK1 via a mutation‐dependent conformational change. This interaction disrupts inhibitory PDPK1 homodimerization and enhances AKT phosphorylation.
Mei Chee Lim   +11 more
wiley   +1 more source

Structure-function insights into the digestive fate of angiotensin-converting enzyme-inhibitory peptides from microwave-treated corn gluten meal. [PDF]

open access: yesFood Chem (Oxf)
Hamzeh A   +7 more
europepmc   +1 more source

ACE inhibition and atherogenesis

Canadian Journal of Physiology and Pharmacology, 2002
Recent clinical studies such as HOPE, SECURE, and APRES show that angiotensin-converting enzyme (ACE) inhibitors like ramipril improve the prognosis of patients with a high risk of atherothrombotic cardiovascular events. Atherosclerosis, as a chronic inflammatory condition of the vascular system, can turn into an acute clinical event through the ...
B A, Schölkens, W, Landgraf
openaire   +3 more sources

Cardiac Effects of ACE Inhibition

Journal of Cardiovascular Pharmacology, 1993
Hypertension frequently is associated with a number of changes in heart structure and function, such as left ventricular hypertrophy, disturbed diastolic function, and subnormal stroke volume during exercise. Most of these changes probably are related to myocardial fibrosis.
P, Lund-Johansen, P, Omvik
openaire   +2 more sources

ACE Inhibition

Circulation, 1997
Background The mechanisms by which ACE inhibitors produce a sustained clinical benefit are not entirely clear but may involve the sympathetic nervous system. We compared the effect of local brachial artery infusions of an ACE inhibitor (perindoprilat) with the effect of placebo (0.9% NaCl) on endogenously mediated (lower body ...
D, Lyons, S, Roy, S, O'Byrne, C G, Swift
openaire   +2 more sources

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