Co

ur
s SC
T
M1
G
F A and signaling
Tyrosine kinase receptors
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 RTKs
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ur
s SC
T
M1
G FA
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 The activation of a receptor protein-tyrosine kinase (RTK)
Co
ur
s SC
T
M1
G FA
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 The activation of a receptor protein-tyrosine kinase (RTK)
Co
ur
s SC
T
M1
G FA
20
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 Co
Activation of RTKs by dimerization
ur
s SC
T
M1
G FA
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Co
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s SC
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M1
G FA
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 Co
Phosphorylated Tyrosines on RTKs Serve as Docking Sites for Intracellular Signaling Proteins

ur
The binding of SH2-containing intracellular signaling

s
proteins to an activated RTK

SC
T
M1
G FA
20
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 Co
Intracellular Signaling Complexes Form at Activated Cell-Surface Receptors

ur
s SC
T
M1
G FA
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Co
ur
s SC
T
M1
G FA
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Co
ur
s SC
T
M1
G FA
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Co
ur
s SC
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M1
G FA
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 Ras activation by RTK
Co
ur
s SC
T
M1
G FA
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Co RTK signaling via RAS/MAPK and PI(3)K pathways

ur
s SC
T
M1
G FA
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Co
ur
s SC
T
M1
G FA
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 Co
ur
s SC
T
M1
G FA
20
Kinase cascade that transmits signals downstream 23
from activated Ras protein to MAP kinase
/20
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Co
ur
s SC
T
M1
G FA
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MAP kinase
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M1
G FA
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 Co
MAPKs are uinvolved
r sS in multiple cellular processes, such as cell
differentiation, proliferation, apoptosis, inflammation, stress
responses, and immune CTdefense.
ERK activation by growth M factors, hormones and proinflammatory
1G
stimuli promotes cell proliferation,

p38 and JNK activation by cellular FAand environmental stresses

promotes multiple cellular processes such as2 proliferation, apoptosis,
02 activity.
immunological effects, insulin signaling and neuronal
3/2
02
4
Co
ur
s SC
T
M1
G FA
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Co
ur
s SC
T
M1
G FA
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 Co
ERK pathway

ur
s SC
T
M1
G FA
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Co
ur
s SC
T
M1
G FA
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Insuline signaling
Co
ur
s SC
T
M1
G FA
20
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 Insuline signaling
Co
ur
s SC
T
M1
G FA
20
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Co RTK signaling via RAS/MAPK and PI(3)K pathways

ur
s SC
T
M1
G FA
20
23
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Co Phosphoinositide 3-kinases (PI3K)

ur
s SC
T
M1
G FA
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Co
ur
s SC
T
M1
G FA
20
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Co
The role of PI 3‐kinase in activating a variety of signaling
pathways
ur
s SC
T
M1
G FA
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 Regulation of glucose uptake in muscle and fat cells by
Co insulin

ur
s SC
T
M1
G FA
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Co
ur
s SC
T
M1
G FA
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 Co
ur
s SC
T
M1
G FA
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TSC : tuberous
sclerosis complex. 24
Examples of Convergence, Divergence, and Cross-Talk Among Signaling
Co
Pathways

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Co
ur
s SC
T
M1
G FA
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Co
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s SC
T
M1
G FA
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MAP kinase transactivation cascades which are triggered by different subtypes of G-protein
alpha subunitsCo
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s SC
T
M1
G FA
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Red lines indicate the inhibitory pathways.
Parallel intracellular signaling

Co
pathways activated by
GPCRs, RTKs, or both
Crosstalk
ur
s SC
T
M1
G FA
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Co
ur
s SC
T
M1
G FA
20
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Genetic analysis reveals the order on which intracellular signaling proteins act in a pathways
Co
ur
s SC
T
M1
G FA
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Genetic analysis reveals the order on which intracellular signaling proteins act in a pathways
Co
ur
s SC
T
M1
G FA
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 Co
A constitutively active form of Ras transmits a signal even in the absence of an extracellular signal

ur
s SC
T
M1
G FA
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 Co Oncogenes
u
A mutated (changed) rsform of a type of gene called a proto-oncogene, which localized in
SCcell growth and division.
virus or is involved in normal
T
When a proto-oncogene is changed M so that too many copies are made or it becomes more
1G
active than normal, it is called an oncogene.

Oncogenes may cause normal cells to become cancer

FAcells and grow in the body.
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23
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24
 Oncogenes: Ras
Co
ur
s SC
T
Ras genes M1
G FA
Ras protein isoforms 20
23
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24
RAS gene mutations
Co
ur
s SC
T
M1
G FA
20 The mutation of a single

23 copy of a proto-
oncogene that converts
/20
it to an oncogene has a
dominant, growth-
24
promoting effect on a
cell
 Co
Ras isoforms are attached to the inner leaflet of the plasma membrane

ur
s SC
T
M1
G FA
Therapeutic target

20
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