16-16: In a series of experiments, genes that code for mutant forms of an RTK are introduced into cells. The cells also express their own normal form of the receptor from their normal gene, although the mutant genes are constructed so that the mutant RTK is expressed at considerably higher concentration than the normal RTK. What would be the consequences of introducing a mutant gene that codes for an RTK (A) lacking its extracellular domain, or (B) lacking its intracellular domain

Question

Biology

Edith Compton

12 February, 05:53

16-16: In a series of experiments, genes that code for mutant forms of an RTK are introduced into cells. The cells also express their own normal form of the receptor from their normal gene, although the mutant genes are constructed so that the mutant RTK is expressed at considerably higher concentration than the normal RTK. What would be the consequences of introducing a mutant gene that codes for an RTK (A) lacking its extracellular domain, or (B) lacking its intracellular domain

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Answers (2)

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Lyric Hanna · Answer 1

(A) lacking its extracellular domain:

RTK receptors can bind to the ligand, this phenomenon leads to a decrease in the rate of molecular interaction between receptors and ligands.

(B) lacking its intracellular domain:

RTK receptors can not bind to the ligand and therefore they are inactive, this phenomenon doesn't have effects on the receptor-ligand interaction mechanism

Explanation:

These types of experiment are very important in molecular biology since they enable to determine the function of transmembrane proteins in molecular signaling pathways

Antwan Roth · Answer 2

Kinase-connected receptors or receptor tyro-sine kinases react for the most part to protein and chemical go between. A solitary trans membrane helix interfaces the extracellular restricting area to the intra-cellular space. e. g. insulin, development factors. The official of the ligand triggers the commencement of a few succession of occasions related with phosphorylation of proteins, this is called protein kinase course.

For instance, the official of development hormone to the receptor in the plasma layer causes dimerization (by the actuation of Janus kinase 2, JAK2) of the receptor (conformation change) that bring about auto-phosphorylation of tyro-sine buildups. The official of SH2-space (src homology) protein (Grb-2) to the phosphorylated tyro-sine buildups invigorates cell development through a course of protein phosphorylation.

a). RTKs are the trans-membrane receptors, which have a ligand restricting site on the extracellular area and tyro-sine authoritative on the intra-cellular space. In the event that it comes up short on the extracellular area, the ligand can't tie to the receptor site, so no cell reaction happens.

b). On the off chance that it does not have the intra-cellular space, the ligand can tie to the receptor site, the receptor can't impart signs tot eh intra-cellular area because of the absence of intra-cellular space.