Ch 15C Assignment Flashcards
Which of these statements about nuclear receptors are true?
They only enter the nucleus after binding to ligand.
They always activate transcription upon binding to ligands in the nucleus.
They can activate or repress transcription based on the type of receptor.
They can activate or repress transcription based on the type of receptor.
PI 3-kinase ……
activates PDK1 by phosphorylating a serine residue on the protein.
is counteracted by PTEN phosphatase.
is only known to be activated by receptor tyrosine kinases.
removes phosphate groups from Serine or Threonine residues.
is counteracted by PTEN phosphatase.
Which of these do not describe Notch?
It is a cell-surface receptor.
Notch tail is released to activate translation.
It is activated by proteolytic processing that involves a series of cleavage steps.
Notch tail is released to activate translation.
Mutations that disrupt the protease activity of gamma-secretase will……………….
inhibit recognition of Notch by Delta.
activate transcription of Notch target genes.
inhibit transcription of Notch target genes.
activate migration of Notch into nucleus.
inhibit transcription of Notch target genes.
Mutations in the SH2 domains of the Grb2 adaptor that inhibit recognition of RTKs will lead to…………………
activation of Sos -GEF.
inhibition of GTP binding to Ras.
exchange of GDP for GTP in Ras.
inhibition of GTP binding to Ras.
Activation of the EGF receptor includes which of these mechanisms?
Phosphorylation by the activator and the receiver.
Conformational change in the receiver.
Phosphorylation of both the monmers by only the activator.
Momomerization of the receptors upon binding to EGF.
Conformational change in the receiver.
In reference to AKT-dependent regulation of Bad, select the statement that is false?
In the absence of a survival signal, Bad is phosphorylated.
In the absence of a survival signal, Bad inhibits the cell-death inhibitor protein Bcl2.
In the presence of a survival signal, Akt is phosphorylated.
In the presence of a survival signal, the cell-death inhibitory protein Bcl2 is active.
In the absence of a survival signal, Bad is phosphorylated.
AKT and ERK activate mTORC1 activity by directly phosphorylating and inhibiting which of these GAPs?
RGS
Gator1
Ras GAPs
TSC
TSC
Upon activation of Ras, the final kinase activated in the MAP Kinase module is………..
Mek
Erk
Raf
MAPKKK
Erk
What of these statements about mTORC1 or mTORC2 are true?
mTORC2 is sensitive to drug rapamycin.
mTORC1 complex activates AKT directly.
mTORC1 is sensitive to rapamycin.
mTORC2 activity is dependent on Rag,
mTORC1 is sensitive to rapamycin.
The GEF that activates Rag GTPase is…………..
Gator1
mTORC1
Rheb
Ragulator
Ragulator
Mutations that inhibit TSC activity leads to the disease- Tuberous Sclerosis that has benign tumors and giant cells and this is due…………..
high mTORC1 activity.
inhibition of mTORC1 activity.
inhibition of AKT.
increased Rheb GTPase activity.
high mTORC1 activity.
Enhancement of Gator1 GAP activity will lead to……………..
inhibition of mTORC1 activity.
activation of mTORC1 activity.
inhibition of mTORC2 activity.
activation of mTORC2 activity.
inhibition of mTORC1 activity.
In the absence of a Wnt signal………….
Beta-catenin is stabilized.
Beta-catenin is degraded.
Beta-catenin accumulates and translocates to nucleus.
LEF1/TCF transcription regulator is activated.
Beta-catenin is degraded.
Degradation of Beta-Catenin by the proteasome is stimulated by………………
disassembly of the APC/Axin degradation complex.
phosphorylation of Beta-Catenin by GSK3 and CK1.
dephosphorylation of Beta-Catenin.
inhibition of GSK3 and CK1 kinases.
phosphorylation of Beta-Catenin by GSK3 and CK1.
