3.3
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In the [REDACTED]trinsic pathway of apoptosis which caspase is activated first? extrinsic intrinsic
When extrinsic pathway is Caspase 8 When intrinsic pathway is Caspase 9
Why is [REDACTED] limited during the execution of apoptosis? atp
mito is destroyed = lower energy
Select the event that is most likely to activate Caspase [REDACTED]. 8 9
DISC apoptosome
Match the cellular feature or event (Hallmark) with the stage of apoptosis: presentation of phosphatidyl serine, fragmentation of DNA caspase 8 or 9 activation of caspase 3 fragmentation / pulling up from cellular surface
Specific activation of Caspase 8 (extrinsic) or 9 (intrinsic) would mark the beginning of apoptosis. b. Activation of Caspase 3, escape of cytochrome C, and possibly the beginning of the loss of PARP are good mid-point indicators of apoptosis. c. Fragmentation, pulling up from cellular surface, presentation of phosphatidyl serine, fragmentation of DNA are all late stage apoptosis indicators.
The liver? [REDACTED]? * Convert __ to __ * Neutralization of __ * Elimination of __
The liver? [REDACTED]? * Convert phenylalanine to tyrosine * Neutralization of lactate * Elimination of nitrogen
What causes gout?
overly active xanthine synthase leads to excess of urate in the blood
A screening of a new born infant patient reveals [REDACTED]. What disease is likely to manifest in this patient? A vanishingly small amount of active hypoxanthine guanine phosphoribosyl transferase, urate, or agressive behavior
Lesch Nyhan syndrome
A screening of a new born infant patient [REDACTED] than considered normal. What disease is likely to manifest in this patient? reveals 75 times more dATP than consider normal
Severe Combined Immunodeficiency
A patient presents with a dietary deficiency of the amino-acid [REDACTED]. What other essential amino-acid needs increased intake to avoid another deficiency? Tyrosine -> Cysteine—>
Tyrosine -> phenylalanine Cysteine—> methionine
A patient with phenylketonuria likely presents with which of the following symptoms? Possible symptoms: ? 4
Neurological damage, an impaired IQ, reduced pigmentation, mental retardation
Consider potential deficiencies of two urea cycle enzymes: [REDACTED]. A person with a [REDACTED] has a life threatening condition. However, a person with [REDACTED] is not life threatening! Why? Carbamoyl Phosphate Synthetase I (CPS1) ; Argininosuccinate Synthetase (ASS)
CPS1– completely blocks the first step of the urea cycle, preventing the removal of toxic ammonia from the blood. deficiency in Argininosuccinate Synthetase (ASS) is not a life-threatening because later steps in the urea cycle, or alternative pathways in the kidneys, can still help excrete nitrogen and manage ammonia levels to some extent