Endocrine Systems and Regulation: Hydrophilic Hormones and Enzyme Cascades

Set of flashcards based on key concepts of hydrophilic hormones and enzyme cascades discussed in the lecture.

What acts on the cells that secrete them, exemplified by T cells and Interleukin-2?

Autocrine hormones.

What type of hormone arises from one cell and acts at a nearby cell?

Paracrine hormones.

What do endocrine hormones do?

They are secreted by endocrine glands, transported in the blood, and act on distant target organs expressing the receptor.

What is the mechanism of juxtacrine signaling?

Juxtacrine signals are transmitted along cell membranes and affect either the emitting cell or adjacent cells.

How are hormones classified based on chemical structure?

Hormones can be amino acid derivatives, peptides and proteins, steroid hormones, or fatty acid derivatives.

What receptors do lipophilic hormones bind to?

Intracellular receptors.

Where do hydrophilic hormones bind?

Cell surface receptors.

What is the key role of cAMP in cellular signaling?

cAMP acts as a second messenger, mediating hormone action inside the cell.

What initiates the MAPK signaling pathway?

The binding of a hormone like EGF to its receptor, leading to receptor dimerization and autophosphorylation.

What function do Sos and Ras serve in cell signaling?

Sos catalyzes the exchange of GDP for GTP on Ras, activating it to initiate signaling cascades.

What is the effect of the activated EGFR in cancer cells?

It can dimerize and send inappropriate signals for growth and division.

What role does Protein Kinase A (PKA) play in cell signaling?

PKA phosphorylates various enzymes, altering cellular metabolism and long-term gene transcription.

What causes the termination of hormonal action in signaling pathways?

Intrinsic GTPase activity of the G protein, phosphodiesterase activity, and action of phosphatases.

What is the action of cholera toxin on G-proteins?

It ADP-ribosylates the α subunit of Gs, blocking GTPase activity and causing continuous activation of adenylate cyclase.

What is the effect of pertussis toxin on G-proteins?

It prevents the displacement of GDP by GTP, blocking the inhibitory action on adenylate cyclase.

How does insulin receptor signaling begin?

By the binding of insulin to the receptor, which triggers cross-phosphorylation of the receptor dimers.

What happens after PIP3 is formed in insulin signaling?

It allows PKB and PDKI to associate with the membrane and become activated.

What is the role of TGF-B receptor in cell signaling?

It activates smad proteins upon phosphorylation, influencing gene expression.

How is insulin signaling linked to the MAPK pathway?

IRS-1 can bind to Grb-2, triggering the activation of the MAPK pathway.

What is the role of G protein-coupled receptor kinases (GRKs) and beta-arrestins in the desensitization of GPCRs?

GRKs phosphorylate activated GPCRs, which then recruits beta-arrestins. Beta-arrestins uncouple the receptor from G proteins, target the receptor for endocytosis, and can initiate alternative signaling pathways (e.g., MAPK)

Outline the key steps involved in the action of a steroid hormone after it binds to its intracellular receptor to modulate gene transcription.

1. Hormone binding to receptor, often releasing heat shock proteins (HSPs). 2. Receptor dimerization. 3. Translocation of the hormone-receptor complex to the nucleus. 4. Binding to hormone response elements (HREs) on DNA. 5. Recruitment of coactivators or corepressors to regulate gene expression

What class of proteins primarily functions as GTPase-activating proteins (GAPs) for G-alpha subunits, thus accelerating the termination of G-protein coupled receptor signaling?

Regulators of G-protein Signaling (RGS) proteins.

In insulin and growth factor signaling, which phosphatase directly antagonizes PI3K activity by dephosphorylating PIP3PIP3 back to PIP2PIP2, and what is its significance as a tumor suppressor?

PTEN (Phosphatase and Tensin homolog). It restricts cell growth and proliferation signals, and loss or mutation of PTEN is a common event in many cancers.

How do nuclear steroid hormone receptors achieve their high specificity in binding to diverse Hormone Response Elements (HREs) on DNA, given the conserved nature of their DNA binding domains?

Specificity is largely determined by the precise nucleotide sequence and spacing of the HRE half-sites, the specific dimerization patterns (homo- or hetero-dimers) formed by the receptors, and the recruitment of distinct coactivator or corepressor proteins that modulate transcriptional outcomes.

Beyond direct enzyme phosphorylation, what is a key nuclear target of Protein Kinase A (PKA) that mediates changes in gene transcription in response to GPCR activation?

PKA phosphorylates CREB (cAMP Response Element-binding protein), which then binds to CRE (cAMP Response Elements) in the promoter regions of target genes, initiating their transcription