Cell Signaling S1M1
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Adenylate cyclase catalyzes the conversion of
ATP to cAMP
Targets of signaling cascades are
- Membrane transporters & ion channels
Steroids enter the cell how
Passive diffusion across the plasma membrane
Are a class of steroid hormones that bind to the glucocorticoid receptor, which is present in almost every vertebrate animal cell
Steroid receptors are unique with
Zinc-finger proteins that function as ligand-activated transcription factors.
What is the pathway for a steriod hormone into the cell
The hormone diffuses across the membrane and binds its receptor in cytoplasm or nucleus.
The hormone-receptor complex binds to response elements in the promoters and enhancers of genes.
This stimulates transcription.
The mechanism for steroid hormones is also used by:
- Retinoic acid (vitamin A)
- Thyroid hormones
- Calcitriol (vitamin D)
Testicular feminization is caused by
A defective androgen receptor
Steroid hormone that stimulates or controls the development and maintenance of male characteristics
Phosphodiesterases (breaks phosphodiester bonds)
A hormone receptor must do what when bonded by a signal molecule
It must change conformation on the cytoplasmic or nuclear side
Water soluble hormones must deliver their message where
To the cell surface
Cyclic AMP is synthesized
From ATP and degraded to AMP
GENE EXPRESSION IS REGULATED BY
PHOSPHORYLATION OF THE TRANSCRIPTION FACTOR CREB
A receptor protein always has how many alpha helices that span the membrane
Once the GDP attaches to the receptor
It changes to GTP (its active state)
How does the GTP prevent from continually sending a signal once it has been triggered
The alpha sub unit turns it off once it binds, turning it back to GDP by hydrolysation
What is the cascade of the cyclic AMP signaling pathway
- 1. A receptor is activated by a signal
- 2. The G protein is activated
- 3. G protein activates Adenylate Cyclcase
- 4. The G protein stops itself from signaling further
- 5. The cyclic AMP activates the protein kinase
- 6. The protein kinase goes around phophorilating proteins
Inhibition of adenylate cyclase
Is pretty much the same cascade as activating only the G protein inhibits the Adenylate cylcase instead of activating it. Both are functioning in the cell at the same time, one just is simply functioning at a higher rate
What if there was no inhibition
Then the cyclase would continue to happen without stopping
Adenylate cyclases are triggered by what
The alpha subunit of the G protein
Cyclic Amp mediates the effects of many
Cyclic adenosine monophosphate (cAMP, cyclic AMP) is
A second messenger important in many biological processes
What is Hormone resistance
When a patient has the hormones, but the effects of the hormones are absent
Patient has signs of chronic PTH (parathyroid hormone) deficiency: hypocalcemia, tetany. But the PTH level is normal or elevated.
Some patients have mutations in the PTH receptor. Others have an abnormal Gs protein that makes inefficient coupling with adenylate cyclase.
Toxic Thyroid Nodules
These are benign tumors in the thyroid gland that overproduce the hormones.
Cause: Some patients have an activating somatic mutation in the gene for the TSH receptor. Others have an activating mutation in the Gs protein that keeps it constitutively active, usually by blocking its GTPase activity.
TSH (Thyroid stimulating hormone) from the pituitary gland stimulates
Hormone production and cell proliferation in the thyroid gland by raising cAMP.
This is an intestinal infection by vibrio cholerae. The bacteria do not invade the tissues, but cause watery diarrhea through a secreted protein toxin.
What happens in cholera toxin
- The toxin enters the cells, and catalyzes the covalent modification of the α-subunit of the Gs protein. This abolishes the GTPase activity of the Gs protein, leaving it in the active state permanently.
- cAMP will accumulate
- Whooping cough:
- Caused by Bordetella pertussis, which lives on the respiratory epithelium. One of its virulence factors is pertussis toxin.
Pertussis toxin mechanism
It modifies the α-subunit of the Gi protein. This inactivates the Gi protein.
Resting calcium is always in what portions of the cell
- Low in the cytoplasm
- High in ER and mitochondria
What is IP3 and DAG
Secondary messengers, molecules used in signal transduction and lipid signaling in biological cells. While DAG stays inside the membrane, IP3 is soluble and diffuses through the cell
Elevations of cytoplasmic calcium can be by
- Hormones acting through a G-protein and IP3
- A ligand-gated ion channel
- Voltage-gated calcium channels
Intracellular calcium receptors include:
- Protein kinase C
- Troponin C
Muscle contraction is always triggered by calcium, but the mechanisms are different in striated muscle and smooth muscle. What is the difference
Striated muscle: Calcium binds to troponin C on the thin filaments.
Smooth muscle: Calcium activates myosin light chain (MLC) kinase.
Membrane-bound guanylate cyclases are activated directly by
Cytoplasmic guanylate cyclase is activated by
Nitric oxide (NO)
Membrane bound guanylate cyclases are activated directly by, whereas cytoplasmic is activated by
Cyclic GMP synthesis
GTP - cGMP - GMP (No G-proteins involved)
What is PKA
Protein Kinase A, it is dependent on cAMP for activation
Calcium contracts vascular smooth muscle triggered by the release of
- (Nor)epinephrine (α1-receptors)
cAMP relaxes vascular smooth muscle triggered by the release of
Atial natriuretic factor receptor (ANF)
A receptor that is ligand activated, activating guanylate cyclase
cGMP relaxes vascular smooth muscle triggered by the release of
- Nitric oxide
- Atrial natriuretic factor (ANF)
Nitrovasodilator drugs (nitroglycerin et al.)
Relax blood vessels because they are metabolized to nitric oxide NO
PDE5 inhibitors (Viagra) inhibit
A cGMP-specific phosphodiesterase in the corpora cavernosa.
Growth factor receptors mediate
Mitogenic and/or growth regulatory effects
Growth factor receptors after binding to the growth factor signal do what
- The receptor autophosphorylates (adds P's)
- Signaling proteins containing an SH2 domain bind to the autophosphorylated receptor.
- The signaling proteins become activated allosterically, or tyrosine-phosphorylated by the receptor.
Insulin receptors are similar to growth factor receptors accept
The unstimulated receptor is a disulfide-bonded tetramer.
Most effects are mediated by IRS-1 and IRS-2.
Infant born without functional insulin receptors.
After Drinking a cup of coffee you get
A more active protein kinase A (PKA)
Steroid Hormone receptor is
A sequence on the DNA that binds to a hormone receptor
Growth factor cascade IP3 system proceeds how
- 1. Formation of IP3: The autophosphorylated receptor phosphorylates and activates phospholipase C-γ (PLC-γ)
- 2. PLC converts PIP2 to IP3
- 3. IP3 triggers calcium release
Activation of protein kinase B growth factors proceeds how
- 1. Autophosphorylated receptor activates PI3K
- 2. This produces PIP3 and 3- phosphorylated inositides
- 3. Insotides activate protein kinase B
The activation of MAP kinases (Growth factor cascade) proceeds how
- 1. Autophosphorylated receptor activates Ras
- 2. Ras activates protein kinases
- 3. Protein kinases phosphorylate and activate MAP kinases
The cascades that are induced by growth factors are out of control in cancer cells. Therefore the best approach for cancer treatment would be a drug that
Inhibits Akt (Protein kinase B)
PTH causes most of its biological effects by stimulating the production of cAMP, the most likely mutation in a patient who has signs of PTH deficiency (hypocalcemia, Tetany,) but an elevated PTH level is
A Gs alpha subunit with a reduced affinity for the PTH receptor
The best way to reduce the cAMP level in the intestinal mucosa is by
How do the second messengers DAG and IP3 differ from the cAMP mechanism
- 1. The GTP Complex cleaves to Phospholipase C
- 2. Phospholipase C forms DAG and IP3
- 3. DAG stays in the membrane and activates Protein Kinase C (PKC)
- 4. IP3 diffuses across the cytoplasm and opens calcium channels in the ER
DAG is short for
PKC is short for
Protein Kinase C
cAMP is triggered by what hormone in the Liver inducing Glycogen breakdown
cAMP is triggered by what hormone in the Adipose tissue inducing Fat breakdown
Epinephrine Beta receptors
cAMP is triggered by what hormone in the Bronchial Smooth muscle inducing Relaxation
Epinephrine beta receptors
cAMP is triggered by what hormone in the vascular smooth muscle inducing Relaxation
Epinephrine beta receptors
TSH does what to the Thyroid gland
Triggers Hormone synthesis
ACTH does what to the Adrenal Gland
Triggers Hormone synthesis
MSH and ACTH does what to the Melanocytes
Triggers Melanin synthesis
Diarrhea is induced by what hormone in the intestines
Opiods do what to the brain and Intestines
Cause constipation in the intestines, and Analgesia (the loss of sense of pain) in the brain
Alpha 2 receptors do what to the brain
Somatostatin has what effect in the pituitary gland
Inhibition of growth hormone secretion
Melatonin has what effect in the melanocytes
It inhibits melanin synthesis
The endothelial cells can act as a vasodilator of vascular smooth muscles when triggered by what
What do endothelial cells release to the smooth muscle causing dilation
NO which turns GTP to cGMP triggering the response
Epinephrine and Prostacyclin trigger what for relaxation in the vascular smooth muscle
Conversion of ATP to cAMP
A specific β-adrenergic receptor kinase that phosphorylates only the activated receptor is
BARK prevents binding of G protein, arrestin follows and degrades it via endocytosis (when degraded, it takes the receptor)
What breaks down cGMP
PDE-5 (Phosphodiesterase 5)
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