Referring to the signalling diagrams, complete the table below. Consider how cell signalling will proceed in a cell exposed to homone H with each of the following homozygous mutations. Mutant csRuactive ? (# refers the HK expressed?Cyclin A cell cycle expressed? progression? compared with cell survival wildtype. to mutants (yes/no) listed above) # 4 (yes/no) (yes/no) (yes/no) (same, more, less) # 5 #1 + #2

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Practice question 1C)
Referring to the signalling diagrams, complete the table below. Consider how cell signalling will
proceed in a cell exposed to hormone H with each of the following homozygous mutations.
Mutant sRuactive ?
(#
refers
the
HK expressed? Cyclin A
cell cycle
expressed? progression? compared with
cell survival
wildtype.
to
mutants (yes/no)
listed
(yes/no)
(yes/no)
(yes/no)
(same, more, less)
above)
# 4
# 5
#1 + #2
Info:
In many mammalian species, including humans, there is a hormone (H) that acts as a key regulator of
hexose (6 carbon sugar, e.g - glucose) metabolism, cell cycle progression, and ultimately cell survival.
Hormone H regulates these effects via its receptors which are found at both the cell surface (csRu)
and within the cell (icRH). The signalling pathways that become activated in the presence of hormone
H are depicted and described below.
hormone
H
extracellular fluid
inactive
GTP
inactive
RAS
Lyn
cell-surface
receptor for H (csR.)
H
icR
GDP
RAS-GTP
hexose
metabolism
cell survival
icRu
G, phase
(resting)
Raf
G,
HK
GSK-3B
MEK
M
G2
hexose kinase
ERK
icR
promoter HRE
COKI
Cyclin A
nucleus
cyclin A
Fos
promoter w a
Created in BioRender.com bio
Transcribed Image Text:Practice question 1C) Referring to the signalling diagrams, complete the table below. Consider how cell signalling will proceed in a cell exposed to hormone H with each of the following homozygous mutations. Mutant sRuactive ? (# refers the HK expressed? Cyclin A cell cycle expressed? progression? compared with cell survival wildtype. to mutants (yes/no) listed (yes/no) (yes/no) (yes/no) (same, more, less) above) # 4 # 5 #1 + #2 Info: In many mammalian species, including humans, there is a hormone (H) that acts as a key regulator of hexose (6 carbon sugar, e.g - glucose) metabolism, cell cycle progression, and ultimately cell survival. Hormone H regulates these effects via its receptors which are found at both the cell surface (csRu) and within the cell (icRH). The signalling pathways that become activated in the presence of hormone H are depicted and described below. hormone H extracellular fluid inactive GTP inactive RAS Lyn cell-surface receptor for H (csR.) H icR GDP RAS-GTP hexose metabolism cell survival icRu G, phase (resting) Raf G, HK GSK-3B MEK M G2 hexose kinase ERK icR promoter HRE COKI Cyclin A nucleus cyclin A Fos promoter w a Created in BioRender.com bio
Signalling via the cell surface receptor
Hormone H mediates its cell cycle stimulatory and pro-survival effects by binding to and
activating the cell surface hormone H receptor (csRu).
The activated csRH activates Lyn, which activates RAS and ultimately the Raf/MEK/ERK
kinase cascade.
Active ERK:
phosphorylates and inactivates GSK-3B. Inhibition of GSK-3B promotes cell survival.
inhibits p27, preventing it from inhibiting cell cycle progression.
activates Fos, a transcription factor which promotes cell cycle progression by triggering
Cyclin A expression.
Signalling via the intracellular receptor
Hormone H also binds to and activates the intracellular hormone H receptor (icRH).
The activated icRH translocates to the nucleus where it acts as a transcription factor binding
to a specific sequence called a hormone H response element (HRE) found within promoters
on the DNA.
İÇRH- HRE binding upregulates the transcription of the hexose kinase gene, which is
required for hexose metabolism and ultimately cell survival.
Below is a list of mutations commonly found in different components of the hormone-signaling
pathways.
Mutant #1: The icRH undergoes a loss-of-function mutation.
Mutant #2: GSK-3B can no longer be phosphorylated.
Mutant #3: ERK is constitutively active.
Mutant #4: Lyn undergoes a gain-of function mutation.
Mutant #5: The cyclin A gene's DNA is highly compacted and inaccessible.
Mutations in the signalling pathways depicted above have been associated with an increased
incidence of several types of cancer.
Transcribed Image Text:Signalling via the cell surface receptor Hormone H mediates its cell cycle stimulatory and pro-survival effects by binding to and activating the cell surface hormone H receptor (csRu). The activated csRH activates Lyn, which activates RAS and ultimately the Raf/MEK/ERK kinase cascade. Active ERK: phosphorylates and inactivates GSK-3B. Inhibition of GSK-3B promotes cell survival. inhibits p27, preventing it from inhibiting cell cycle progression. activates Fos, a transcription factor which promotes cell cycle progression by triggering Cyclin A expression. Signalling via the intracellular receptor Hormone H also binds to and activates the intracellular hormone H receptor (icRH). The activated icRH translocates to the nucleus where it acts as a transcription factor binding to a specific sequence called a hormone H response element (HRE) found within promoters on the DNA. İÇRH- HRE binding upregulates the transcription of the hexose kinase gene, which is required for hexose metabolism and ultimately cell survival. Below is a list of mutations commonly found in different components of the hormone-signaling pathways. Mutant #1: The icRH undergoes a loss-of-function mutation. Mutant #2: GSK-3B can no longer be phosphorylated. Mutant #3: ERK is constitutively active. Mutant #4: Lyn undergoes a gain-of function mutation. Mutant #5: The cyclin A gene's DNA is highly compacted and inaccessible. Mutations in the signalling pathways depicted above have been associated with an increased incidence of several types of cancer.
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