Catalytic Receptor and Steroid Receptor Signaling

Vocabulary flashcards covering key concepts from Module 2 Lecture 7 on Catalytic Receptor and Steroid Receptor Signaling, including kinase domains, adaptor proteins, signaling pathways, insulin action, and steroid receptor mechanisms.

Catalytic Receptors

Transmembrane receptor proteins that transmit intracellular signals via phosphorylation of tyrosine residues, using either intrinsic tyrosine kinase activity or associated non-receptor intracellular tyrosine kinases.

Adaptor Proteins

Intracellular signaling molecules with conserved domains that bind phosphotyrosine residues on catalytic receptor tails to link activated receptors to downstream signaling pathways.

SH2 Domain

Src homology 2 domain; a highly conserved structural region in adaptor proteins that specifically recognizes and docks at phosphotyrosine residues on cytoplasmic receptor tails.

Ras

A small GTP-binding protein homologous to the ̢\alpha subunit of heterotrimeric G proteins that acts as a molecular switch to trigger the MAP kinase cascade, with constitutively active mutant forms present in approximately $30\%$ of tumors.

MAP Kinase Cascade

A Serine/Threonine phosphorylation cascade activated downstream of Ras that culminates in mitogen-activated protein kinase (MAPK) translocating to the nucleus to phosphorylate transcription factors.

STATs

Signal transducers and activators of transcription; latent SH2-containing cytoplasmic proteins that dock at phosphotyrosines, undergo tyrosine phosphorylation by receptor kinases, dimerize, and translocate to the nucleus to stimulate gene transcription.

PI3 Kinase Pathway

A major signaling pathway where activated PI3 kinase converts membrane $PIP_2$ to $PIP_3$, creating docking sites to recruit and activate Akt, which phosphorylates Bad to promote cell survival.

PTEN

A phosphatase enzyme that dephosphorylates membrane inositol phospholipids like $PIP_3$ back to $PIP_2$, effectively terminating PI3 kinase pathway signaling.

Non-receptor Tyrosine Kinases

Cytoplasmic tyrosine kinases (such as Src and Janus Kinases) that non-covalently bind to receptor cytoplasmic tails lacking intrinsic catalytic activity, such as cytokine and growth hormone receptors.

Insulin Receptor

A pre-formed catalytic receptor with intrinsic tyrosine kinase activity that does not require independent chains to join after ligand binding and acts by phosphorylating insulin receptor substrates (IRS).

Insulin Receptor Substrates (IRS)

Target proteins (IRS-1, IRS-2, IRS-3, IRS-4) that are tyrosine-phosphorylated by the activated insulin receptor kinase to propagate downstream metabolic and growth signals.

Nuclear-Initiated Steroid Signaling (NISS)

Classical steroid signaling mechanism where lipid-soluble hormones diffuse across the plasma membrane to bind intracellular cytosolic or nuclear receptors that act as ligand-activated transcription factors.

Membrane-Initiated Steroid Signaling (MISS)

Rapid steroid signaling mechanism mediated by membrane-associated steroid receptors in caveolae, producing cellular responses within seconds to minutes by modifying existing proteins without new protein synthesis.

Caveolae

Invaginated domains of the plasma membrane where membrane-associated steroid receptors are localized to initiate rapid MISS responses.

Steroid Hormone Receptor Structure

An intracellular protein construct featuring an $NH_2$-terminal gene regulatory domain, a central DNA-binding domain, a hinge region, and a $COOH$-terminal hormone-binding domain.