#Question id: 1250
#Unit 4. Cell Communication and Cell Signaling
Few mutants (column A) and their results (column B) are listed in the table given below:
|
Column A |
Column B |
|
A. Gain-of-function of Ski |
I. Inhibits the ability of activated type I TGF-β receptors (RI) to phosphorylate R-Smad proteins |
|
B. Loss-of-function of RII receptor |
II. Transcription activation induced by TGF-β and mediated by Smad complexes is shut down |
|
C. Gain-of-function of smad-7 |
|
|
D. Loss-of-function of R-smad |
Match the correct mutation with the observe result?
#Question id: 1251
#Unit 4. Cell Communication and Cell Signaling
Following statements are regarding to receptor serine kinases.
A. The two serines in each Smad3 that were phosphorylated by the RI receptor kinase bind to phosphoserine-binding sites in the MH1 domains of a Smad3 or a Smad4, forming a stable complex containing two molecules of phosphorylated Smad3 (or Smad2) and one molecule of the co-Smad (Smad4).
B. The bound importin then mediates translocation of the heteromeric R-Smad/co-Smad complex into the nucleus.
C. After importin dissociates inside the nucleus, the Smad3/Smad4 (or Smad2/Smad4) complex binds to other transcription factors to activate transcription of specific target genes.
D. Transcription of the PAI-1 gene requires formation of a complex of the transcription factor TFE3 with the R-Smad/co-Smad (Smad3/Smad4) complex and binding of all these proteins to specific sequences within the regulatory region of the PAI-1 gene.
E. Within the nucleus, R-Smads are further modified by phosphorylation of their linker domains, monoubiquitinylation of their MH1 domains, acetylation of their MH2 domains, and dephosphorylation of the C-terminal serines by nuclear phosphatases.
Which of the following combination is incorrect?
#Question id: 1252
#Unit 4. Cell Communication and Cell Signaling
Following statements are regarding to the phosphoinositide signaling pathway.
A. Many RTKs and cytokine receptors can initiate the IP3/ DAG signaling pathway by activating phospholipase Cβ (PLCβ), a different PLC isoform.
B. Activated RTKs and cytokine receptors also can initiate another phosphoinositide pathway by binding a PI-3 kinase, thereby allowing the enzyme access to its membrane-bound phosphoinositide substrates, which then become phosphorylated at the 3 position.
C. Protein kinase B (PKB) becomes partially activated by binding to PI 3-phosphates with its PH domain.
D. Full activation of PKB requires phosphorylation by the kinase PDK1, which is also recruited to the membrane by binding to PI 3-kinase, and by a second kinase, PDK2.
Which of the following combination is incorrect?
#Question id: 1253
#Unit 4. Cell Communication and Cell Signaling
Following statements are regarding to the wnt signalling.
A. Wnt proteins interact with several cell-surface proteins and activate multiple downstream signal transduction pathways. The principal signaling receptor for Wnt proteins is Frizzled (Fz), which contains seven transmembrane α helices.
B. The palmitate attached to the Wnt protein binds to a specific site on the Fz intracellular domain and stabilizes the Wnt-Fz complex.
C. “canonical” Wnt signaling pathway uses a second transmembrane protein, LRP, that associates with Frizzled in a Wnt signal– dependent manner.
D. In the resting state, two kinases in the complex, casein kinase 1 (CK1) and GSK3, sequentially phosphorylate β-catenin on multiple tyrosine residues.
Which of the following statements are correct?
#Question id: 1254
#Unit 4. Cell Communication and Cell Signaling
An inhibitor of phosphodiesterase activity would have which of the following effects?
#Question id: 1255
#Unit 4. Cell Communication and Cell Signaling
Following statements are regarding to the mechanism of action of cholera toxin.
A. cholera toxin is a homodimeric protein, target G proteins, interfering with normal signaling in host cells.
B. cholera toxin associates with a small G protein, known as ARF6.
C. association with ARF6 activates cholera toxin, which catalyzes the transfer of ADP-ribose from NAD+ to the critical Arg residue in the P loop of the alpha subunit of Gs.
D. ADP-ribosylation blocks the GEF activity of Gs and thereby renders Gs permanently inactive.
E. This results in continuous activation of the adenylyl cyclase of intestinal epithelial cells, chronically high cAMP, and active PKA dephosphorylates the CFTR Cl- channel and a sodium-proton exchanger in the intestinal epithelial cells.
Which of the following combination is correct?