I believe the answer you are looking for is "Cytoskeleton".
Answer:
Answer explained
Explanation:
a. Overexpression of Axl receptor tyroxine kinase correlates with the decresed patient's overall survival and hence it's inhibition is under process.
AXL TKI BMS777607 treatment increased AXL protein levels after 24 h as observed by Western blot and flow cytometry analysis. Mechanistically, this inhibition-induced AXL cell surface accumulation was neither associated with epigenetic modifications, nor altered transcriptional and translational regulation. Hence this later increased the glycosylated protien abundance in kinase dead mutant. The kinase function blockaging resulted in impaired internalisation which finally incresed the level of proliferation.
An alternative technique may exist in linkage of Axl Tkl to a degradation machinery recruitment unit .
b. Mendelian disorders like cystic fibrosis results from error in the given DNA sequence which can be autosomal dominant and recessive both and also X or Y linked. Mutated gene results in the Mendelian disorders. Whereas in cancer there can be mutation or proliferation of the given cells in a specific area. In cancer cells there is 2.5 times more the mRNA present while 6.2times the DNA and hence the detection and diagnosis automatically becomes difficult as in Mendelian disorders only single sequence needs to be studied at a time .
The gradual cooling if the body after death is ALGOR MORTIS
