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Malate accumulation and transcriptome patterns during fruit development in sweet Cherry (Prunus avium L.). [PDF]

BMC Plant Biol
Liu C, Chen L, Qi X, Song L, Wang M, Han S, Li M.   +6 more
europepmc   +1 more source

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Regulation of mTOR by phosphatidic acid

Trends in Endocrinology & Metabolism, 2023
mTORC1, the mammalian target of rapamycin complex 1, is a key regulator of cellular physiology. The lipid metabolite phosphatidic acid (PA) binds to and activates mTORC1 in response to nutrients and growth factors. We review structural findings and propose a model for PA activation of mTORC1.
Maria A. Frias, Ahmet Hatipoglu, David A. Foster   +2 more
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Regulation of Bile Acid Biosynthesis

Current Pharmaceutical Design, 1997
Abstract: An elevated concentration of low density lipoprotein (LDL) cholesterol is an independent risk factor for cardiovascular disease. The only quantitatively significant way by which cholesterol is removed from the body is via the bile, either directly or after conversion to bile acids. Therapeutic modalities which increase bile acid biosynthesis,
Princen, H.M.G., Post, S.M., Twisk, J.
openaire   +2 more sources

Regulation of the proteome by amino acids

PROTEOMICS, 2016
Besides their main contribution as substrates for protein synthesis, amino acids as signaling molecules could exert some regulatory functions on protein synthesis and/or proteolysis that have been emphasized in a number of recent studies. Several publications have highlighted supplemental roles of those amino acids in protein metabolism as well as in ...
Bourgoin-Voillard, Sandrine, Goron, Arthur, Seve, Michel, Moinard, Christophe   +3 more
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Regulation of bile acid synthesis

Hepatology, 1991
HEPATIC CHOLESTEROL HOMEOSTASIS The liver plays a central role in the regulation of cholesterol homeostasis. Under normal conditions, cholesterol input into the body equals output; cholesterol homeostasis is maintained. Under pathologic conditions, enhancement of cholesterol input into the liver or a reduction in hepatic cholesterol output may ...
Z R, Vlahcevic, D M, Heuman, P B, Hylemon   +2 more
openaire   +2 more sources

Regulation of Gastric Acid Secretion

Annual Review of Physiology, 1979
The three stimulants of gastric acid secretion likely to have physiological roles in regulation of secretion are acetylcholine, gastrin, and histamine. Acetylcholine is released by vagal and intramucosal reflex stimulation, acting directly on the parietal cell.
A H, Soll, J H, Walsh
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Regulation of Gastric Acid Secretion

Current Opinion in Gastroenterology, 1998
This paper summarizes important developments, published over the past year, that improve our understanding of the regulation of gastric acid secretion at the central, peripheral, and intracellular levels and mechanisms by which various neurotransmitters, paracrine agents, and hormones regulate gastric secretion and are themselves regulated.
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The Regulation of Retinoic Acid Formation

Nutrition Reviews, 2009
Rat liver microsomal as well as cytosolic retinol dehydrogenases from cellular retinal-binding protein (CRBP)-retinal from CRBP-retinol. A cytosolic dehydrogenase transforms retinal into retinoic acid. Apo-CRBP and ethanol inhibit the cytosolic but not the microsomal retinol dehydrogenase, the latter being the primary enzyme in the rate-limiting step ...
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Acid-base regulation in pregnancy

American Journal of Physiology-Legacy Content, 1976
Plasma bicarbonate decreases during normal pregnancy. To assess what roles increased extra cellular volume or alterations in parathyroid hormone levels (iPTH) have in the maintenance of this decrement, we evaluated acid-base metabolism in eleven 3rd-trimester women. Base-line pH and PCO2 were 7.44 and 27.3 mmHg, respectively. Mean tubular reabsorption
V S, Lim, A I, Katz, M D, Lindheimer
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Acid-base regulation by the kidneys

The American Journal of Medicine, 1950
Abstract The kidney participates in the regulation of body neutrality by stabilizing the plasma concentration of bicarbonate-bound base at a level of 25 to 27 mEq. /L. The respiratory system participates by stabilizing the plasma carbonic acid level at 1.25 to 1.35 mEq. /L.
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