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Comprehensive vocabulary flashcards covering micronutrients, nucleotide metabolism pathways, signal transduction systems, bioenergetics, and redox homeostasis based on lecture notes.
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Thiamine Pyrophosphate (TPP)
The active coenzyme form of Vitamin B1 involved in decarboxylation reactions, serving as an essential cofactor for pyruvate dehydrogenase, α-ketoglutarate dehydrogenase, and transketolase.
Megaloblastic Anemia
A hematologic disorder caused by Folate (B9) or Vitamin B12 deficiency that impairs one-carbon unit transfer, halting dTMP synthesis and causing nuclear maturation in rapidly dividing hematopoietic cells to lag behind cytoplasmic growth.
Vitamin D
A fat-soluble steroid-like hormone that undergoes sequential activation in the skin, liver, and kidney to regulate intracellular receptors controlling Ca2+/PO4 homeostasis and bone mineralization.
γ-Carboxylation
A Vitamin K-dependent post-translational modification of glutamate residues on coagulation proteins that creates the Ca2+ binding sites necessary for effective hemostasis.
PRPP (Phosphoribosyl Pyrophosphate)
The universal activated ribose-phosphate scaffold onto which purine rings are built atom-by-atom and to which pre-assembled pyrimidine rings are attached.
Inosine Monophosphate (IMP)
The central branch-point nucleotide intermediate produced at the end of de novo purine synthesis, from which the pathways to synthesize AMP and GMP diverge.
Lesch-Nyhan Syndrome
A severe metabolic disorder caused by a genetic deficiency in the purine salvage enzyme HGPRT, preventing the economic recovery of preformed purine bases.
Thymidylate Synthase
The enzyme that catalyzes the conversion of dUMP to dTMP using a THF-derived one-carbon donor, serving as a key target for anti-cancer therapeutics.
Uric Acid
The relatively insoluble final product of purine degradation in humans, high levels of which cause hyperuricemia and urate crystal deposition leading to gouty arthritis.
G Protein-Coupled Receptors (GPCRs)
A major class of cell-surface receptors that, upon ligand binding, activate heterotrimeric G-proteins to generate second messengers such as cAMP or IP3.
Receptor Tyrosine Kinases (RTKs)
Cell-surface receptors that undergo ligand-induced dimerization and autophosphorylation on tyrosine residues, initiating intracellular kinase cascades like PI3K-Akt and Ras-MAPK.
JAK-STAT Pathway
A cytokine receptor signaling pathway lacking intrinsic kinase activity that recruits Janus Kinases (JAKs) to phosphorylate STAT transcription factors for direct gene regulation.
Inositol 1,4,5-Trisphosphate (IP3)
A soluble second messenger produced by PLC-β cleavage of PIP2 that binds receptors on the Endoplasmic Reticulum to trigger a rapid release of cytosolic Ca2+.
Catabolism
The metabolic pathway network that oxidizes complex nutrient molecules to extract energy, yielding ATP, NADH, and FADH2, active primarily during the fasting state.
Anabolism
The metabolic pathway network that consumes ATP and simple precursor molecules to synthesize complex macromolecules such as glycogen, proteins, and lipids during the fed state.
Complex I (NADH Dehydrogenase)
The primary respiratory chain complex that accepts high-energy electrons from NADH and pumps protons from the mitochondrial matrix into the intermembrane space.
Complex II (Succinate Dehydrogenase)
The mitochondrial electron transport chain complex that accepts electrons from FADH2 but lacks proton-pumping capability.
Complex IV (Cytochrome c Oxidase)
The terminal respiratory chain complex that transfers electrons to molecular oxygen to yield water (O2+4e−+4H+→2H2O) while pumping protons into the intermembrane space.
Chemiosmotic Coupling
The process by which the energy of the electrochemical proton gradient drives protons back into the mitochondrial matrix exclusively through the Fo component of ATP Synthase to synthesize ATP.
Cyanide Poisoning
Toxicological inhibition of Complex IV in the electron transport chain that directly halts electron transfer, proton pumping, and cellular ATP synthesis.
Thermogenin (UCP1)
An uncoupling protein found in brown adipose tissue that forms an alternative proton pore in the inner mitochondrial membrane, dissipating the proton gradient as heat.
Superoxide (O2∙−)
A true free radical containing an unpaired electron, generated when electrons prematurely leak from Complexes I and III of the electron transport chain and partially reduce molecular oxygen.
Superoxide Dismutase (SOD)
A Zinc/Copper-dependent antioxidant enzyme that converts superoxide radicals into hydrogen peroxide (H2O2) and molecular oxygen.
Glutathione Peroxidase
A Selenium-dependent antioxidant enzyme that detoxifies hydrogen peroxide (H2O2) into water using reduced glutathione (GSH).
Glutathione (GSH)
A tripeptide molecule serving as the principal intracellular reducing system by donating reducing equivalents to peroxides, requiring NADPH-dependent regeneration from GSSG.
Ischemia-Reperfusion Injury
Pathological cellular damage resulting when restored oxygen delivery to ischemic tissues causes damaged mitochondria and recruited immune cells to generate a massive burst of ROS.