Signal Transduction Lecture - Fill-in-the-Blank Flashcards

Flashcards cover key signaling pathways and mechanisms from GPCR, RTK, NO-cGMP, Wnt/β-catenin, NF-κB, and RhoA/ROCK, as described in the lecture notes.

In this patient with melanoma and a V600E BRAF mutation treated with Vemurafenib, the drug's mechanism is __.

Inhibiting the activity of the V600E variant of BRAF.

Mutations in BRAF are found in _% of melanoma.

40-60%

Ligand for RTK

GF, mem bound organelles

Adaptor proteins such as Grb2 and SOS activated by phosphorylated RTK facilitate the activation of , a small GTP-binding protein.

RAS

Ras signal cascade

RTK, RAS, RAF, MEK, ERK

RAF kinases phosphorylate and activate , which then phosphorylates ERK.

MEK

Activated ERK phosphorylates transcription factors such as .

Ets, Fos, Elk1, and MYC

The first membrane signaling step in GPCR Gq signaling is activation of , which hydrolyzes PIP2 into DAG and IP3.

phospholipase C-β (PLC-β)

IP3 triggers Ca²⁺ release and, together with DAG, activates .

protein kinase C (PKC)

Protein regulating Grb2, SOS

NF1

Cholera toxin ADP-ribosylates the Gsα subunit, locking it in the active GTP state and constitutively activating .

adenylate cyclase

Cholera toxin mechanism differs from Gq signaling because Gq activates PLC to make IP3/DAG, while Gs activates to raise cAMP.

adenylate cyclase (cAMP production)

NO is synthesized by endothelial NOS (eNOS) from the amino acid .

arginine

NO activates soluble guanylate cyclase to produce the second messenger , which activates PKG.

cGMP

In atherosclerosis, reduced NO bioavailability leads to diminished cGMP production and decreased signaling via .

cGMP-PKG signaling

In the canonical Wnt pathway, the OFF state keeps β-catenin by the destruction complex.

degraded

In the ON state of Wnt signaling, stabilized β-catenin accumulates and translocates to the nucleus to interact with to activate transcription.

TCF

Wnt signaling drives Myc activation via transcription.

β-catenin/TCF-mediated

The best etiology for acromegaly is that the pituitary adenoma causes increased release of growth hormone, resulting in elevated .

IGF-1

Activation of α1‑adrenergic receptors signals via to produce IP3 and DAG, leading to Ca²⁺ release and PKC activation.

phospholipase C (PLC)

β-adrenergic receptors are Gs-coupled GPCRs; their activation increases , which in turn activates PKA.

cAMP

NF-κB activation via the canonical pathway involves cytokines triggering the IKK complex to phosphorylate IκB, leading to its degradation and the release of NF-κB that translocates to the nucleus to .

drive transcription of NF-κB–dependent genes

RhoA-GTP activates ROCK, which inhibits phosphatase, increasing MLC phosphorylation and smooth muscle contraction.

myosin light chain phosphatase (MLCP)