Thewke 3

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heat chaperone proteins

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are sometimes associated with the Gluccocorticoid receptor.

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response elements for steroid hormones are

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either direct repeats or inverted repeats.

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steroid receptro class forms

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homodimers that bind to resposne elements.

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RXR partnered receptors

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form heterodimers that bind diret repeats

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orphan class

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of NR from homodimers that bind direct repeats

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glucs can supress

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by binding to negative GREs

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Domain structure NR

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n terminal has a transactivation function. a well conserved central dan binding domain containing two zinc finger motiffs. a large c terminal ligand hormone binding domain which varies substantially

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DNA binding domain contains

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two sets of four cysteine residues and each set chelates a zinc ion froming loops zing fingers.... mediate specificity in binding to HRE.

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thus the zinc fingers

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mediate specificty in binding to HREs hormone response elements, module binding site.

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Agents that bind to the hormone binding site have been used to clinically modulate hormone acticity.

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yep

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tamoxifen

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competes with estrogen for binding to the estrogen receptor, but the tamoxifen receptor complex is inactive. treats breast cancer

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RU846

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is used for early termination of pregnancy by binding to progesterone receptor

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chlomiphene

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binds to the hypothalamic estrogen receptor causing release of GnRH. THis stimulates LH and FSH. treats infertillity

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gene activation by NR

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is due to the recruitment of coactivators by the hormone receptro complex.

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Interference

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is due to the prevention of coactivaotrs antagonist receptor complex

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gene repression or silencing

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due to the recuitment of repressors by some nuclear receptors in the absence of the hormone like thyroid and retinoic

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binding in ligand domain of NR

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acts like a switch to turn on

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steroid receptor coactivators src

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have Histone acetyltransferase activities, acetylation of chrmatin makes more active dna

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binding to ere of ligand

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causes homodimerization and translocation to the nucleius. causes src recruit via nuclear receptor interacting domain. brings in others and transcription is upregualted

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ligand binding in the estrogen receptor

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allows co-activator interaction

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recurrent breast cancer shows

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resistance to tamoxifen about 50%. Resistance is not associated with ERa but with PKA activation.

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tamoifen resistant breast cancer

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has a PKA subunit (R) that is not expressed as much and so PKA is always active and this phosphorylates the ERa receptor residue serine 305. this prevents the formation fo the tamoxifen inactive complex. IN fact, now tamoxifen induces trascription like estrogen ---growth stimulation of tumor.

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NR gene promoters may have a negative response element

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and when levels of horome are tow high this may regulate expression by NR-complex binding and prevent over stimulation

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nr complex may also activate

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genes that inhibit expression of nr gene, so like negtive feedback.

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klinefeleters

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fsh and lh elevated and testosterone is subnormal xxy

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turners syndrome

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elevated plasma FSH and prepbuertal estradiol

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polycystic ovary

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hypersecretion of androgens

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sometimes autoantibodies to TSH receptor

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activate it an and patient has hyperthyroidism. or if the antibody does not stimulate the receptor then hypothyroidism

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generalized thyroid hormone resistance have been found

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and have mutations in the thryoid hormone receptor which aboloish ligan binding. Have elevated levels of everything but receptor fucked. Dominant is mutant gene interfering with function, recessive are due to a deletion of the THRb gene.

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NR receptor dysfunction clinically

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horomone levels are elevated, sometimes high doses can cure.

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Gluco receptor def.

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have mutations that lead to reduced receptor binding and have addision like disease state but elevated levels of cortisol and in urine, or a decrease in binding to the DNA for receptro.

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eclampsia

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hypertension in pregnancy

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hypertension can occur in pregancny

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and may be associated with ser180 to leu mutation in the MR gene. This new product is constituitively active somewhat and also binds progesterone.

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eicosanoids.

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are most often concerned with immune, clotting, or inflammation becasue they can be mobilized rapidly.

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eicosanoids are lipid derived but

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bind to g-protein coupled receptors and modulate adenylate cyclase or PLC.

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prostanoids

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prostaglandins and thromboxanes are autocrine and paracrine.

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leukotrienes

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relatively stable and long lived molecules. mediate recruitement of neutrophils and eosoniphils. Are the slow reacting substance of anaphylaxis. SRS-a

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SRS-a why lueks

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cause slowly evlovling but protracted contraction of smooth muslce in airways and GI tract. responsible for bronchoconstriction in astham. release by mast cells in allergic response after binding of the appropriate Ige tot eh antigen.

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singulair is leuk receptor

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antagonsit. leuks receptros are GPCRs.

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15-d-PGj2 binds to a nuclear hormone called PPARy that work with peroxisome ......and is

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is imporant for adipogenesis. upon activation PPary heterodimerizes with the RXR and binds to DNA seq. called PPRE that activate target genes encoding enzyme for lipid metabolism

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PAF

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is synthesized and released by polymorphonuclear leukocytes and endothelial cells during acute inflamm response. Extremely potent. ether linkage at sn-1 and acetyl at sn-2.The Paf receptor is a GPCR coupled to Gq.

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lysophosphatidic acid and sphingosine-1-phosphate

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imp. for growth responses and cellular effector responses that depend cytoskeletal responses.

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SIP binds to

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members of the endothelial differentiation gene.

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edg receptro family are

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demonstrated to be GPCR coupled to specific downstream stuff including calcium mobilazation, mapk, or adenylate cyclase. USead against hyperproliferative skin disease.

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ceramidase

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makes sphingosine from ceramides. sphingosine kinase Ps u know.

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lysophospholipase D removes the choline groupabove named but with choline in name and

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LPA acts as a potent mitogen due to its inactivation of three high affinity G protein coupled receptors called LPA1 through 3. also known as EDG 2 4 and 7. Linked to cancer.

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NO made by many cells

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and is synthesized by the deamination of arginine catalyzed by the enzyme NO synthase. a

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NO

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activates soluable form of guanylate cyclase making cGMP which acts as a second messenger.

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NO signaling causes smooth muslce relaxation

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nitroglycerine converted to NO and increase blood flow in vessels.

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soluable guanylate cyclase is a dimeric complex of distinct a and b subunits and each intact dimer constituitively binds a molecule of heme. IN the absence of NO this enzyme has low activity. soooo

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binding of NO to heme group induces conformational changes that greatly increase catlaytic activity and the prod. of cGMP

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cGMP phosphodiesterase

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degrades cGMP.

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viagra inhibts

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type 5 PDE that is highly expressed in vascular smooth muscle and viagra is 80 to 4000 fold less potent as an inhibitor of other types of PDE like pde3 in cardiac muscle.

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viagra is selective for PDE6

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which is the signal protein for transducin in the retina and can cause vision problems. Some temporary blindiness with viagra.