Answer:
2.5 ft and 24 in cubed your welcome
Explanation:
:)
Answer:
The process of cell division will slow down and the cell will die
Explanation:
Without the golgi apparatus or if its not working as well as it should be there would be no lysosomes or less. Without the lysosomes there will be a lot of junk/trash in the cell and it would have no way to break it down and get it out
Answer:
A dominant phenotype will be expressed when at least one allele of its associated type is present, whereas a recessive phenotype will only be expressed when both alleles are of its associated type. However, there are exceptions to the way heterozygotes express themselves in the phenotype.
Explanation:
Sorry idk My bad I just need points for my calculus assignment
Answer:
The correct insulin pathway is described as under:
2. Binding of insulin to the alpha subunit of the insulin receptor
8. Activation of insulin receptor tyrosine kinase
3. Phosphorylation of IRS proteins
6. Phosphorylation of phosphinositide 3-kinase (PI-3K)
4. Conversion of PIP2 to PIP3
7. Activation of PIP3-dependent protein kinase B (PDK1)
5. Glut4 receptors transported to the cell membrane
Explanation:
The insulin signaling pathway is described as under:
RTK (receptor tyrosine kinases) which is a receptor for insulin is an extracellular receptor but in contrast to other cell surface receptors it is catalytic in nature. In the absence of insulin (ligand), it is monomeric but as soon as it gets activated (activation occurs upon ligand binding), it undergo dimerization. It leads to auto-phosphorylation in it's tyrosine residue which subsequently leads to phosphorylation of tyrosine residue of other receptors. Such hyper-phosphorylated receptor have high affinity with enzyme/molecule like IRS protein which have SH2 domain . IRS down stream activates phosphinositide 3-kinase (PI-3K). This enzyme converts component of animal cell membrane PIP2 into PIP3. PIP3 also remains membrane bound but it has the potential to phosphorylate another enzyme named as PIP3-dependent protein kinase B (PDK1). Further, PDK1 leads to the activation of Akt or PK-B. Akt is a serine-threonine kinase which ultimately leads to the recruitment of Glut4 receptors on cell membrane for uptake of more and more glucose into the cell.
Note: Apart from this Akt also phosphorylates another protein named as FOXO which ultimately causes cell growth, Akt can also phosphorylate BAD protein so as to restrict cell apoptosis or we can say it leads to cell survival, Akt also leads to translation in a cell with the help of mTOR raptor etc.
