Neurotensin receptor: Difference between revisions
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The ligand for NTSR1 is the 13 amino acid peptide, neurotensin (NTS)<ref name="SONT">PMID:23051748</ref>, and the majority of the effects of NTS are mediated through NTSR1<ref name="SONT"/>. NTS has a variety of biological activities including a role in the '''[https://en.wikipedia.org/wiki/Leptin leptin]''' signaling pathways <ref name="Mice">PMID: 20211191</ref>, tumor growth <ref name="cancer">PMID:16887236</ref>, and '''[https://en.wikipedia.org/wiki/Dopamine dopamine]''' regulation <ref name="Schizophrenia">PMID:22596253</ref>. NTSR1 was crystallized bound with a C-terminal portion of its tridecapeptide '''[https://en.wikipedia.org/wiki/Ligand ligand]''', <scene name='72/721548/Neurotensin/7'>NTS(8-13)</scene>. The shortened ligand was used because of oits higher potency and efficacy than its full-length counterpart<ref name="SONT"/>. | The ligand for NTSR1 is the 13 amino acid peptide, neurotensin (NTS)<ref name="SONT">PMID:23051748</ref>, and the majority of the effects of NTS are mediated through NTSR1<ref name="SONT"/>. NTS has a variety of biological activities including a role in the '''[https://en.wikipedia.org/wiki/Leptin leptin]''' signaling pathways <ref name="Mice">PMID: 20211191</ref>, tumor growth <ref name="cancer">PMID:16887236</ref>, and '''[https://en.wikipedia.org/wiki/Dopamine dopamine]''' regulation <ref name="Schizophrenia">PMID:22596253</ref>. NTSR1 was crystallized bound with a C-terminal portion of its tridecapeptide '''[https://en.wikipedia.org/wiki/Ligand ligand]''', <scene name='72/721548/Neurotensin/7'>NTS(8-13)</scene>. The shortened ligand was used because of oits higher potency and efficacy than its full-length counterpart<ref name="SONT"/>. | ||
A critical topic in the understanding of GPCRs is the transition from the inactive to active state. This transition is responsible for the [https://en.wikipedia.org/wiki/Signal_transduction transduction] of a signal from the extracellular to the intracellular space. The transition occurs when a ligand, NTS in the case of NTSR1, binds to the receptor causing a [https://en.wikipedia.org/wiki/Conformational_change conformational change] that leads to the activation of the intracellular G protein. Currently, only the structure of the active form of NTSR1 is known, making the transition between the active and inactive states difficult to study.<ref name="SONT"/> | A critical topic in the understanding of GPCRs is the transition from the inactive to active state. This transition is responsible for the [https://en.wikipedia.org/wiki/Signal_transduction transduction] of a signal from the extracellular to the intracellular space. The transition occurs when a ligand, NTS in the case of NTSR1, binds to the receptor causing a [https://en.wikipedia.org/wiki/Conformational_change conformational change] that leads to the activation of the intracellular G protein. Currently, only the structure of the active form of NTSR1 is known, making the transition between the active and inactive states difficult to study.<ref name="SONT"/> | ||
*'''Neurotensin receptor 1''' is involved in the regulation of blood presure, body temperature, weight and response to pain<ref >PMID:31243364</ref> | |||
*'''Neurotensin receptor 3''' may serve as a scavenger receptor to eliminate neutotensin from the extracellular fluid and trigger its degradation<ref >PMID:11257441</ref> | |||
See also [[Transmembrane (cell surface) receptors]] | |||
== Neurotensin == | == Neurotensin == | ||
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**[[6os9]], [[6osa]] - hNTR1 (mutant) in GI1 complex – human – Cryo EM<br /> | **[[6os9]], [[6osa]] - hNTR1 (mutant) in GI1 complex – human – Cryo EM<br /> | ||
**[[5t04]] - rNTR1 + peptide - rat<br /> | **[[6pwc]] - hNTR1 + neurotensin peptide + arrestin + antibody – Cryo EM<br /> | ||
**[[7ul2]] - hNTR1 + nanobody – Cryo EM<br /> | |||
**[[6up7]] - hNTR1 + peptide + arrestin – Cryo EM<br /> | |||
**[[6z66]] - rNTR1 - rat<br /> | |||
**[[5t04]], [[6z4v]] - rNTR1 + peptide - rat<br /> | |||
**[[4xee]], [[4xes]], [[4grv]] - rNTR1 + neurotensin peptide<br /> | **[[4xee]], [[4xes]], [[4grv]] - rNTR1 + neurotensin peptide<br /> | ||
**[[3zev]], [[4buo]], [[4bv0]], [[4bwb]] - rNTR1 (mutant) + neurotensin peptide<br /> | **[[3zev]], [[4buo]], [[4bv0]], [[4bwb]] - rNTR1 (mutant) + neurotensin peptide<br /> | ||
**[[7l0p]], [[7l0q]], [[7l0r]], [[7l0s]] - rNTR1 (mutant) + neurotensin peptide + Gi – Cryo EM<br /> | |||
**[[8fmz]], [[8fn0]] - rNTR1 (mutant) + neurotensin peptide + Gi + scfV – Cryo EM<br /> | |||
**[[8fn1]] - rNTR1 + neurotensin peptide + Gi + scfV – Cryo EM<br /> | |||
**[[6z4q]], [[6z4s]], [[6z8n]], [[6za8]], [[6zin]] - rNTR1 + agonist<br /> | |||
**[[6yvr]] - rNTR1 + peptide agonist<br /> | |||
* Neurotensin receptor 3 (sortilin) | * Neurotensin receptor 3 (sortilin) | ||
**[[6eho]] – hNTR3 Vps10P domain (mutant) | **[[6eho]] – hNTR3 Vps10P domain (mutant) <br /> | ||
**[[4po7]] – hNTR3 Vps10P domain + neurotensin/neuromedin N peptide<br /> | **[[4po7]] – hNTR3 Vps10P domain + neurotensin/neuromedin N peptide<br /> | ||
**[[3f6k]] – hNTR3 Vps10P domain + neurotensin peptide <br /> | **[[3f6k]] – hNTR3 Vps10P domain + neurotensin peptide <br /> | ||
**[[4msl]] – hNTR3 Vps10P domain + ligand<br /> | **[[4msl]] – hNTR3 Vps10P domain + ligand<br /> | ||
**[[6x3l]], [[6x48]], [[6x4h]] – hNTR3 Vps10P domain + inhibitor<br /> | |||
**[[4n7e]] – hNTR3 Vps10P domain (mutant) + inhibitor<br /> | **[[4n7e]] – hNTR3 Vps10P domain (mutant) + inhibitor<br /> | ||
**[[5mrh]], [[5mri]] – hNTR3 Vps10P domain + triazolone<br /> | **[[5mrh]], [[5mri]] – hNTR3 Vps10P domain + triazolone<br /> | ||
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[http://proteopedia.org/wiki/index.php/User:R._Jeremy_Johnson/CH462:Biochemistry_II_Butler_University Butler University Proteopedia Pages] | [http://proteopedia.org/wiki/index.php/User:R._Jeremy_Johnson/CH462:Biochemistry_II_Butler_University Butler University Proteopedia Pages] | ||
See also: | |||
*[[Receptor]] | |||
*[[Transmembrane (cell surface) receptors]] | |||
*[[G protein-coupled receptors]] | |||
== References == | == References == |