Answer: There is presence of tumor.
Explanation: The adhesion of cells to extracellular matrix (EMC) through integrins ( cell-EMC binding molecules, which are collagens, laminins and fibronectin) causes the activation of kinases in the cytoplasm.
However, kinanes helps in controlling the epithelial cell differentiation and upholding the epithelial tissues. This is done by the addition of phosphate groups to a substrate protein which is termed Protein phosporylation. Then, the kinases direct the affairs of the cell and it's activities. For example, it determines the cell division, anabolic and catabolic activities of the cell, movement of ions between the cell and it's environment (signal transduction), protein functions and etc.
Conclusively, since the activities of the cell like cell division and protein functions is dictated by the kinase, reduction in cell division that gave rise to rapid growth is put on hold. Hence, the tumor is been suppressed.
Note: the binding of cell-EMC is regulated by Transforming Growth Factor (TGF) β.
The correct answer is the last statement.
If the regulatory serine is mutated to alanine, then acetyl-CoA carboxylase will get activated spontaneously and will produce malonyl-CoA. The increased concentrations of malonyl-CoA will obstruct the oxidation of fatty acids by preventing the entry of fatty acids into the mitochondria.
It is because the AMP-activated protein kinase phosphorylates the serine residues of acetyl-CoA carboxylase to inactivate it. If a mutation occurs in such residues, then the AMPL cannot phosphorylate acetyl-CoA carboxylase and this enzyme will get activated spontaneously.
In such a situation, there will be more than sufficient production of malonyl-CoA, which will inhibit the admittance of more fatty acid getting inside the mitochondria; this will indirectly prevent the oxidation of fatty acids.
