This is all in the attached folder as well for proper formatting. You will be introduced toSerine-Threonine Kinase-coupled receptors and the signal transduction pathwaysthey initiate. I'm attaching...

Function of Smad:
Smad 2 found on the chromosome 18q21 and it is present near the Smad 4 locus in the genome of humans. The mutation studies identified that 6% of the colon cancer is caused due to the missense mutation either in the MHCI or MHC II of the Smad 2. By the process of immunostaining it is identified that 70% of human skin SCCs show the reduce production of this protein or loss of tumor tissues. The loss of Smad2 protein is higher in the poorly differentiated SCCs. The Smad2 does not directly bind with the DNA molecule but it complexes with both Smad3 and Smad4. Thus binding of snail to the SBE leads to the recruitment of Smad4 through the binding of snail with Smad3. This process in turn leads to the contribution of EMT. The Smad2 deficient skin is more susceptible for the formation of skin tumors and for the conversion of malignant one. The loss of Smad 2 will up regulate the activities of Smad3 and 4 and binds with the SBE of snail and HGF. Hence it leads in the increased production of snail and HGF is said to be induced by Smad2 deletion induced tumorogenesis.
Smad 3 is in the chromosome of 15q21 – 22 chromosomes in human. It is frequent in the human colon cancer and in breast cancers. However the Smad3 production is not lost in skin SCCs where as the increased expression of it is expressed in breast cancer. TGF – beta over expression and followed inflammation is induced by TPA contributes greatly towards the tumor development. Studies indicate that the Smad3 has its own tumor suppression function through Smad3 mediated TGF – beta function. It is said as the major mediator for TGF – beta, Smad3 may either acts as a tumor suppressor or tumor promoter in context dependent manner.
Smad 4 is identified with the tumor suppressor function in pancreatic cancers. Now it is characterized as the major mediator of TGF – beta signaling. Germ line mutation of Smad4 induces juvenile polyposis syndrome. Loss of heterozygosity had reported in many tumors. Analysis indicates that the loss of Smad4 has been associated in the inactivation of PTEN and P21 ,it promotes cell proliferation and it inhibits apoptosis in cells and it is interrelated with TGF – beta induced inflammation hence it accelerates tumor development and the proliferation of the same.
General mechanism of signal transduction:
GF – beta signaling controls most of the cellular events like regulation of the embryonic process, immunological, tumor regulation and wound healing, etc. GF-beta is functioned by the binding of the ligand molecules to the cell membrane receptor, thus it activates the cytoplasmic mediators in to the nucleus and thus finally it regulates the expression of their target gene. The ligand is three forms and as TGF-beta 1, 2, 3. The cell surface receptors are as TGF-beta RI and R2. Usually the Smad signaling from the cytoplasm to the nucleus can performed by three Smad isomers of the family and it can be said as Smad 2, 3, 4. Binding of the ligand with TGF-beta R2 - R1, phosphorylation of Smad2 and Smad3, it binds with Smad4 and forms trimeric complex, translocated to...