The steps for protein synthesis in order are:
1. Copy of one side of DNA strand is made (called mRNA, messenger RNA)
2. mRNA moves to cytoplasm, then ribosome.
3. mRNA goes through ribosome 3 bases at a time.
4. transfer RNA (tRNA) matches up with the open DNA bases.
5. tRNA releases the amino acid at the top, which joins the chain of amino acids being produced.
When mRNA exits the nucleus, it travels to a ribosome, which is made up of proteins and rRNA. The ribosome reads the mRNA's codon sequence. The correct sequence of amino acids is delivered to the ribosome by tRNA molecules. A ribosome is responsible for translating the codons in mRNA into a chain of amino acids.
Initiation, elongation, and termination are the three main stages of translation. The small subunit and the big subunit are two distinct subunits that make up the ribosome. The tiny subunit binds to the mRNA's 5' end during initiation.
Then it shifts in a 5' x 3' direction. The TR when RNA that has an amino acid linked to it binds to the mRNA. They participate in translation because they are molecules that are involved in protein synthesis, which is translation. And those molecules that link the minor assets Holden's RNA from M. with. The mRNA is now bound to the tRNA by antipodean.
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The best and most correct answer among the choices provided by the question is the third choice "<span>Epigenetic changes of mother cells are generally maintained in daughter cells; however, they are susceptible to environmental influences." </span>I hope my answer has come to your help. God bless and have a nice day ahead!
Long-term potentiation (LTP) is considered a cellular correlate of learning and memory. The presence of G protein-activated inwardly rectifying K(+) (GIRK) channels near excitatory synapses on dendritic spines suggests their possible involvement in synaptic plasticity. However, whether activity-dependent regulation of channels affects excitatory synaptic plasticity is unknown. In a companion article we have reported activity-dependent regulation of GIRK channel density in cultured hippocampal neurons that requires activity oF receptors (NMDAR) and protein phosphatase-1 (PP1) and takes place within 15 min. In this study, we performed whole-cell recordings of cultured hippocampal neurons and found that NMDAR activation increases basal GIRK current and GIRK channel activation mediated by adenosine A(1) receptors, but not GABA(B) receptors. Given the similar involvement of NMDARs, adenosine receptors, and PP1 in depotentiation of LTP caused by low-frequency stimulation that immediately follows LTP-inducing high-frequency stimulation, we wondered whether NMDAR-induced increase in GIRK channel surface density and current may contribute to the molecular mechanisms underlying this specific depotentiation. Remarkably, GIRK2 null mutation or GIRK channel blockade abolishes depotentiation of LTP, demonstrating that GIRK channels are critical for depotentiation, one form of excitatory synaptic plasticity.
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The heart must beat faster during exersise because by increasing the heart rate the body is able to increase cardiac output and deliver the necessary blood flow to the mucles
