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A glycogen storage disease is a metabolic disorder caused by a deficiency of an enzyme or transport protein affecting glycogen synthesis, glycogen breakdown, or glucose breakdown, typically in muscles and/or liver cells.
In cell biology, protein kinase A (PKA) is a family of serine-threonine kinase whose activity is dependent on cellular levels of cyclic AMP (cAMP). PKA is also known as cAMP-dependent protein kinase. PKA has several functions in the cell, including regulation of glycogen, sugar, and lipid metabolism. It should not be confused with 5'-AMP-activated protein kinase.
5' AMP-activated protein kinase or AMPK or 5' adenosine monophosphate-activated protein kinase is an enzyme that plays a role in cellular energy homeostasis, largely to activate glucose and fatty acid uptake and oxidation when cellular energy is low. It belongs to a highly conserved eukaryotic protein family and its orthologues are SNF1 in yeast, and SnRK1 in plants. It consists of three proteins (subunits) that together make a functional enzyme, conserved from yeast to humans. It is expressed in a number of tissues, including the liver, brain, and skeletal muscle. In response to binding AMP and ADP, the net effect of AMPK activation is stimulation of hepatic fatty acid oxidation, ketogenesis, stimulation of skeletal muscle fatty acid oxidation and glucose uptake, inhibition of cholesterol synthesis, lipogenesis, and triglyceride synthesis, inhibition of adipocyte lipogenesis, inhibition of adipocyte lipolysis, and modulation of insulin secretion by pancreatic β-cells.
Exercise intolerance is a condition of inability or decreased ability to perform physical exercise at the normally expected level or duration for people of that age, size, sex, and muscle mass. It also includes experiences of unusually severe post-exercise pain, fatigue, nausea, vomiting or other negative effects. Exercise intolerance is not a disease or syndrome in and of itself, but can result from various disorders.
Glycogen synthase is a key enzyme in glycogenesis, the conversion of glucose into glycogen. It is a glycosyltransferase that catalyses the reaction of UDP-glucose and n to yield UDP and n+1.
Mitochondrial myopathies are types of myopathies associated with mitochondrial disease. Adenosine triphosphate (ATP), the chemical used to provide energy for the cell, cannot be produced sufficiently by oxidative phosphorylation when the mitochondrion is either damaged or missing necessary enzymes or transport proteins. With ATP production deficient in mitochondria, there is an over-reliance on anaerobic glycolysis which leads to lactic acidosis either at rest or exercise-induced.
Myophosphorylase or glycogen phosphorylase, muscle associated (PYGM) is the muscle isoform of the enzyme glycogen phosphorylase and is encoded by the PYGM gene. This enzyme helps break down glycogen into glucose-1-phosphate, so it can be used within the muscle cell. Mutations in this gene are associated with McArdle disease, a glycogen storage disease of muscle.
Peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α) is a protein that in humans is encoded by the PPARGC1A gene. PPARGC1A is also known as human accelerated region 20 (HAR20). It may, therefore, have played a key role in differentiating humans from apes.
Protein kinase C epsilon type (PKCε) is an enzyme that in humans is encoded by the PRKCE gene. PKCε is an isoform of the large PKC family of protein kinases that play many roles in different tissues. In cardiac muscle cells, PKCε regulates muscle contraction through its actions at sarcomeric proteins, and PKCε modulates cardiac cell metabolism through its actions at mitochondria. PKCε is clinically significant in that it is a central player in cardioprotection against ischemic injury and in the development of cardiac hypertrophy.
Mitochondrially encoded 12S ribosomal RNA is the SSU rRNA of the mitochondrial ribosome. In humans, 12S is encoded by the MT-RNR1 gene and is 959 nucleotides long. MT-RNR1 is one of the 37 genes contained in animal mitochondria genomes. Their 2 rRNA, 22 tRNA and 13 mRNA genes are very useful in phylogenetic studies, in particular the 12S and 16S rRNAs. The 12S rRNA is the mitochondrial homologue of the prokaryotic 16S and eukaryotic nuclear 18S ribosomal RNAs. Mutations in the MT-RNR1 gene may be associated with hearing loss. The rRNA gene also encodes a peptide MOTS-c, also known as Mitochondrial-derived peptide MOTS-c or Mitochondrial open reading frame of the 12S rRNA-c.
Casein kinase II subunit beta is a protein that in humans is encoded by the CSNK2B gene. It is a ubiquitous protein kinase which regulates metabolic pathways, signal transduction, transcription, translation, and replication. The enzyme localizes to the endoplasmic reticulum and the Golgi apparatus.
5'-AMP-activated protein kinase catalytic subunit alpha-2 is an enzyme that in humans is encoded by the PRKAA2 gene.
Pyruvate dehydrogenase lipoamide kinase isozyme 4, mitochondrial (PDK4) is an enzyme that in humans is encoded by the PDK4 gene. It codes for an isozyme of pyruvate dehydrogenase kinase.
Pyruvate dehydrogenase kinase isoform 2 (PDK2) also known as pyruvate dehydrogenase lipoamide kinase isozyme 2, mitochondrial is an enzyme that in humans is encoded by the PDK2 gene. PDK2 is an isozyme of pyruvate dehydrogenase kinase.
Fibronectin type III domain-containing protein 5, the precursor of irisin, is a type I transmembrane glycoprotein that is encoded by the FNDC5 gene. Irisin is a cleaved version of FNDC5, named after the Greek messenger goddess Iris.
Pinchas Cohen is the dean of the USC Leonard Davis School of Gerontology, holds the William and Sylvia Kugel Dean's Chair in Gerontology and serves as the executive director of the Ethel Percy Andrus Gerontology Center.
Humanin is a micropeptide encoded in the mitochondrial genome by the 16S ribosomal RNA gene, MT-RNR2. Its structure contains a three-turn α-helix, and no symmetry.
Small humanin-like peptides (SHLPs) are a group of peptides encoded in the 16S ribosomal RNA region of mitochondrial genome. Six peptides of this group (SHLP1–6) have been identified so far, each peptide is of 20-38 amino-acid long. They are derived from the mitochondria and act as important retrograde signaling molecules in the cell. Their names were given because the SHLPs share some similar biological effects with the mitochondrial peptide Humanin.
David A. Hood is a Canadian exercise physiologist and Director of the Muscle Health Research Centre at York University, Toronto, Canada. He is a professor and holder of an NSERC Tier I Canada Research Chair in Cell Physiology. Hood is credited with making significant research advances in understanding of the biology of exercise, mitochondria and muscle health.
Dimitri Krainc is the Aaron Montgomery Ward Professor and Chairman of the Ken & Ruth Davee Department of Neurology and Director of the Simpson Querrey Center for Neurogenetics at Northwestern University Feinberg School of Medicine. He completed his research and clinical training at the Massachusetts General Hospital and Harvard Medical School, where he served on faculty until relocating to Northwestern in 2013. He was awarded the Javits Neuroscience Investigator Award and outstanding investigator award from NIH, and is President-elect of the American Neurological Association. Krainc was elected to the Association of American Physicians and the National Academy of Medicine for what NAM described as “groundbreaking discoveries in the area of neurodegenerative disorders." He is the principal founding scientist of biotech companies Lysosomal Therapeutics and Vanqua Bio and serves as Venture Partner at OrbiMed.
References
- ↑ Lee, Changhan; Kim, Kyung Hwa; Cohen, Pinchas (1 November 2016). "MOTS-c: A novel mitochondrial-derived peptide regulating muscle and fat metabolism". Free Radical Biology and Medicine. 100: 182–187. doi:10.1016/j.freeradbiomed.2016.05.015. ISSN 0891-5849. PMC 5116416 . PMID 27216708.
- ↑ Dieli-Conwright, Christina M.; Sami, Nathalie; Norris, Mary K.; Wan, Junxiang; Kumagai, Hiroshi; Kim, Su-Jeong; Cohen, Pinchas (19 August 2021). "Effect of aerobic and resistance exercise on the mitochondrial peptide MOTS-c in Hispanic and Non-Hispanic White breast cancer survivors". Scientific Reports. 11 (1): 16916. Bibcode:2021NatSR..1116916D. doi:10.1038/s41598-021-96419-z. ISSN 2045-2322. PMC 8376922 . PMID 34413391.
- ↑ Kumagai, Hiroshi; Kim, Su-Jeong; Miller, Brendan; Natsume, Toshiharu; Lee, Shin Hyung; Sato, Ayaka; Ramirez, Ricardo; Wan, Junxiang; Mehta, Hemal H; Yen, Kelvin; Cohen, Pinchas (May 2023). "Casein kinase 2 is a direct binding partner and a functional target of the exercise-mimetic microprotein MOTS-c". Physiology. 38 (S1). doi:10.1152/physiol.2023.38.S1.5725846. ISSN 1548-9213. S2CID 258979715.
- ↑ Wan, Wei; Zhang, Lieliang; Lin, Yue; Rao, Xiuqing; Wang, Xifeng; Hua, Fuzhou; Ying, Jun (2023). "Mitochondria-derived peptide MOTS-c: effects and mechanisms related to stress, metabolism and aging". Journal of Translational Medicine. 21 (1): 36. doi: 10.1186/s12967-023-03885-2 . PMC 9854231 . PMID 36670507.
- ↑ "Explanation of Key Changes on the 2024 WADA Prohibited List". 13 October 2023. Retrieved 6 December 2023.