Podcast
Questions and Answers
What is the initial interaction in the JAK-STAT mechanism?
What is the initial interaction in the JAK-STAT mechanism?
What happens after STATs are tyrosine-phosphorylated by JAKs?
What happens after STATs are tyrosine-phosphorylated by JAKs?
Which condition results from non-functional JAK3?
Which condition results from non-functional JAK3?
What is a consequence of mutations in STAT1 and STAT2?
What is a consequence of mutations in STAT1 and STAT2?
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What has overexpression of STAT3 been associated with?
What has overexpression of STAT3 been associated with?
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Which cytokines signal through JAK3?
Which cytokines signal through JAK3?
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What role does STAT4 play in diseases?
What role does STAT4 play in diseases?
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How are non-functional cytokine receptors related to psoriasis?
How are non-functional cytokine receptors related to psoriasis?
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What is the final step in the JAK-STAT mechanism before target gene transcription?
What is the final step in the JAK-STAT mechanism before target gene transcription?
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What leads to the dissociation of STATs from the receptor in the JAK-STAT mechanism?
What leads to the dissociation of STATs from the receptor in the JAK-STAT mechanism?
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Which condition can result from non-functional JAK3?
Which condition can result from non-functional JAK3?
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What is the function of activated STATs in the JAK-STAT mechanism?
What is the function of activated STATs in the JAK-STAT mechanism?
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In which disease are STAT4 mutations often associated?
In which disease are STAT4 mutations often associated?
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What is a consequence of mutations in STAT1 and STAT2?
What is a consequence of mutations in STAT1 and STAT2?
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Which condition can arise due to overexpression of STAT3?
Which condition can arise due to overexpression of STAT3?
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What can non-functional cytokine receptors lead to?
What can non-functional cytokine receptors lead to?
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Study Notes
Cell Division and Signaling Pathways
- Cells divide to replace old or damaged cells, grow, and increase in size.
- Cell growth, differentiation, and proliferation are crucial for organism development and maintenance.
Cell Signaling
- Cell signaling is the ability of cells to receive, process, and transmit signals with their environment and themselves.
- Signals can be physical (mechanical pressure, voltage, temperature, light) or chemical (small molecules, peptides, or gas).
- Signaling molecules can be synthesized through various biosynthetic pathways and released through passive or active transport, or from cell damage.
Signaling Pathways
- 17 signaling pathways mentioned, including:
- Akt/PKB
- AMPK
- cAMP-dependent
- Wnt
- Eph/ephrin
- Hippo
- Insulin signal transduction
- JAK-STAT
- MAPK/ERK
- mTOR
- Nodal
- Notch
- PI3K/AKT/mTOR
- TGF beta
- TLR
- VEGF
- Hedgehog
Wnt Signaling Pathway
- A group of signal transduction pathways that begin with proteins passing signals into cells through cell surface receptors.
- Wnt signaling pathways use paracrine or autocrine communication.
- Wnt signals give shape to tissues as cells proliferate.
- Misregulation of Wnt signaling can lead to tumor development via excess cell proliferation.
Wnt/β-Catenin Pathway (Canonical Pathway)
- Wnt signaling begins with Wnt protein binding to the Frizzled (Fz) family receptor.
- Co-receptors (LDL receptor-related protein 5/6) may be required alongside the Wnt protein and Fz receptor interaction.
- The signal is transmitted to Disheveled (Dsh), a protein located in the cytoplasm.
- Wnt causes the translocation of the negative Wnt regulator, Axin, and the destruction complex (APC and GSK) to the plasma membrane.
- β-Catenin accumulates and localizes to the nucleus, inducing a cellular response via regulating transcription of target genes.
JAK-STAT Signaling Pathway
- JAK-STAT signaling allows the transcription of genes involved in cell division.
- Excessive JAK-STAT signaling can lead to cancer formation.
- JAK-STAT signaling in mammary glands promotes cell division and reduces cell apoptosis, causing cancer breast.
- High STAT3 activity plays a major role in this process, allowing the transcription of genes involved in cell division.
- Mutations in JAK2 cause leukemia and lymphoma.
JAK-STAT Mechanism
- The binding of cytokines (interleukin and interferons) to cell surface receptors causes the receptors to dimerize, bringing the receptor-associated JAKs into close proximity.
- JAKs phosphorylate each other through transphosphorylation, increasing their kinase domain activity.
- Activated JAKs then phosphorylate tyrosine residues on the receptor.
- STATs bind to the phosphorylated tyrosine on the receptor and are tyrosine-phosphorylated by JAKs, causing the STATs to dissociate from the receptor.
- Activated STATs form hetero or homodimers, translocating to the nucleus to induce transcription of target genes.
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Description
Learn about the key players and interactions in the Wnt signaling pathway, including the role of co-receptors like LDL receptor-related protein 5/6 and the interaction between Wnt protein, Fz receptor, and Disheveled (Dsh) protein. Understand how signals are transmitted within the pathway.
