Govt. Exams
Entrance Exams
Ubiquitin is a 76-amino acid protein that is conjugated to lysine residues of target proteins via E1, E2, and E3 enzymes, marking them for degradation by the 26S proteasome.
Gaucher disease results from deficiency of β-glucosidase (glucocerebrosidase), leading to accumulation of glucocerebroside in lysosomes, particularly in macrophages, spleen, and liver.
In α-helix, hydrogen bonds form between C=O and N-H groups within the same chain. In β-sheet, hydrogen bonds form between adjacent polypeptide chains running parallel or antiparallel to each other.
In competitive inhibition, the inhibitor competes with substrate for the active site, so more substrate is needed to achieve half-maximal velocity (increased apparent Km), but Vmax remains unchanged.
Km is the substrate concentration at which the reaction velocity is half of Vmax (V = Vmax/2), and it represents the affinity of enzyme for substrate. Lower Km indicates higher affinity.
The Lineweaver-Burk plot is a double reciprocal plot where 1/v is plotted against 1/[S], allowing easy determination of Km (x-intercept) and Vmax (y-intercept) from linear regression.
Chaperone proteins like HSP70 and HSP90 facilitate proper protein folding, prevent aggregation, and assist in maintaining protein stability, though some also work with degradation pathways.
Cooperative binding (positive cooperativity) occurs when binding of one substrate molecule enhances the affinity of the enzyme for additional substrate molecules, as seen in hemoglobin and phosphofructokinase.
Cytochrome c oxidase contains heme a, heme a3, and copper centers (CuA and CuB) essential for electron transfer and oxygen reduction.
Hyperammonemia type 1 (Reye's syndrome-like) results from CPS I deficiency, the first enzyme in the urea cycle. CPS I catalyzes ammonia fixation to form carbamoyl phosphate. Its deficiency prevents ammonia detoxification, causing neurotoxic accumulation.
