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Welcome to wherearetheanswers’s page.
Contributor score: 9


Comments ...

 +2  (nbme19#49)

Another tRNA has to attach to the A site before the peptide chain can be hydrolyzed from the P site and moved to the A site tRNA (FA 2020 pg 45)

fataldose  As the Peptide chain is transfered to the tRNA at the A site, the ribosome moves down the mRNA moving the now empty P site tRNA to the E site, and the tRNA from the A site to the P site, making room for the next amino acid charged tRNA to attach to the A site. Additional points- The translation comes to an end when a releasing factor recognizes one of the stop codons (does not code for an amino acid), which then catalyzes the release of the peptide chain from the tRNA in the P site. Peptidyl transfer to E site is wrong because peptidyl tranfer occurs between P site to the A site, not to the E site eIF4E is a eukaryotic translation initiation factor involved in directing ribosomes to the cap structure of mRNAs. Once methionine charged tRNA locates the start codon, all initiation factors are released. +3

 +1  (nbme19#39)

The kidneys make glucose too? 6 years of studying science and no one mentions the kidneys.





Subcomments ...

submitted by shaikh(-1),

competitive ACh antagonist blocks muscular and neuronal activity thus no respiratory in and out flow, no muscular activity

wherearetheanswers  I get why tubocurarine would cause this, but can someone explain why it also couldn't be tetrodotoxin? +1  
wherearetheanswers  Actually some googling helped! In case anyone else is wondering, tubocurarine acts at the NMJ so you would get continued phrenic nerve depolarization like you see in the figure. Conversely, tetrodotoxin works at sodium channels which are on axons so blockade of this would result in decreased phrenic nerve activity as well. +5  


submitted by shaikh(-1),

competitive ACh antagonist blocks muscular and neuronal activity thus no respiratory in and out flow, no muscular activity

wherearetheanswers  I get why tubocurarine would cause this, but can someone explain why it also couldn't be tetrodotoxin? +1  
wherearetheanswers  Actually some googling helped! In case anyone else is wondering, tubocurarine acts at the NMJ so you would get continued phrenic nerve depolarization like you see in the figure. Conversely, tetrodotoxin works at sodium channels which are on axons so blockade of this would result in decreased phrenic nerve activity as well. +5