Gi alpha subunit: Difference between revisions

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* [[Histamine]] [[Histamine H3 receptor|H<sub>3</sub>]] & [[Histamine H4 receptor|H<sub>4</sub>]] receptors
* [[Histamine]] [[Histamine H3 receptor|H<sub>3</sub>]] & [[Histamine H4 receptor|H<sub>4</sub>]] receptors
* [[Melatonin]] [[MTNR1A|MT<sub>1</sub>]], [[MTNR1B|MT<sub>2</sub>]], & [[MTNR1C|MT<sub>3</sub>]] receptors
* [[Melatonin]] [[MTNR1A|MT<sub>1</sub>]], [[MTNR1B|MT<sub>2</sub>]], & [[MTNR1C|MT<sub>3</sub>]] receptors
* Hydroxycarboxylic acid receptors [[Niacin receptor 1|HCA2]] & [[Niacin receptor 2|HCA3]]
* [[Hydroxycarboxylic acid receptors]]: [[HCA1]], [[HCA2]], & [[HCA3]]
* [[Opioid]] [[Delta Opioid receptor|δ]], [[Kappa Opioid receptor|κ]], [[Mu Opioid receptor|μ]], & [[Nociceptin receptor|nociceptin]] receptors
* [[Opioid]] [[Delta Opioid receptor|δ]], [[Kappa Opioid receptor|κ]], [[Mu Opioid receptor|μ]], & [[Nociceptin receptor|nociceptin]] receptors
* [[Prostaglandin]] [[PTGER1|EP<sub>1</sub>]], [[PTGER3|EP<sub>3</sub>]], [[FP receptor|FP]], & [[Thromboxane receptor|TP]] receptors
* [[Prostaglandin]] [[PTGER1|EP<sub>1</sub>]], [[PTGER3|EP<sub>3</sub>]], [[FP receptor|FP]], & [[Thromboxane receptor|TP]] receptors
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G<sub>i</sub> mainly inhibits the [[cAMP dependent pathway]] by inhibiting adenylate cyclase activity, decreasing the production of [[Cyclic adenosine monophosphate|cAMP]] from [[Adenosine triphosphate|ATP]], which, in turn, results in decreased activity of [[cAMP-dependent protein kinase]]. Therefore, the ultimate effect of G<sub>i</sub> is the opposite of [[function of cAMP-dependent protein kinase|cAMP-dependent protein kinase]].
G<sub>i</sub> mainly inhibits the [[cAMP dependent pathway]] by inhibiting adenylate cyclase activity, decreasing the production of [[Cyclic adenosine monophosphate|cAMP]] from [[Adenosine triphosphate|ATP]], which, in turn, results in decreased activity of [[cAMP-dependent protein kinase]]. Therefore, the ultimate effect of G<sub>i</sub> is the opposite of [[function of cAMP-dependent protein kinase|cAMP-dependent protein kinase]].


It is also attributed a minor role in activation of the [[phospholipase C pathway]].<ref>{{cite journal |vauthors=Obál F, Krueger J | title = The somatotropic axis and sleep. | journal = Rev Neurol (Paris) | volume = 157 | issue = 11 Pt 2 | pages = S12–5 | year = 2001 | pmid = 11924022}}</ref> Growth hormone is required for normal postnatal growth, bone growth, regulatory effects on protein, carbohydrate, and lipid metabolism.<ref name=GeneGlobe>[https://www1.qiagen.com/GeneGlobe/PathwayView.aspx?pathwayID=199 GeneGlobe -> GHRH Signaling]{{dead link|date=October 2017 |bot=InternetArchiveBot |fix-attempted=yes }} Retrieved on May 31, 2009</ref> although this is mainly a function of the [[Gq alpha subunit|G<sub>q</sub> alpha subunit]].
It is also attributed a minor role in activation of the [[phospholipase C pathway]].<ref>{{cite journal |vauthors=Obál F, Krueger J | title = The somatotropic axis and sleep. | journal = Rev Neurol (Paris) | volume = 157 | issue = 11 Pt 2 | pages = S12–5 | year = 2001 | pmid = 11924022}}</ref> Growth hormone is required for normal postnatal growth, bone growth, regulatory effects on protein, carbohydrate, and lipid metabolism.<ref name=GeneGlobe>[https://www1.qiagen.com/GeneGlobe/PathwayView.aspx?pathwayID=199 GeneGlobe -> GHRH Signaling]{{dead link|date=October 2017 |bot=InternetArchiveBot |fix-attempted=yes }} Retrieved on May 31, 2009</ref> Although this is mainly a function of the [[Gq alpha subunit|G<sub>q</sub> alpha subunit]].


== Types ==
== Types ==

Latest revision as of 09:24, 10 January 2019

G protein subunit alpha i1
Identifiers
SymbolGNAI1
Entrez2770
HUGO4384
OMIM139310
PDB3UMR
RefSeqNM_002069
UniProtP63096
Other data
LocusChr. 7 q21-q22
G protein subunit alpha i2
Identifiers
SymbolGNAI2
Entrez2771
HUGO4385
OMIM139360
RefSeqNM_002070
UniProtP04899
Other data
LocusChr. 3 p21
G protein subunit alpha i3
Identifiers
SymbolGNAI3
Entrez2773
HUGO4387
OMIM139370
PDB2ODE
RefSeqNM_006496
UniProtP08754
Other data
LocusChr. 1 p13
G protein subunit alpha o1
Identifiers
SymbolGNAO1
Entrez2775
HUGO4389
OMIM139311
RefSeqNM_020988
UniProtP09471
Other data
LocusChr. 16 q13

Gi alpha subunit (Gαi, or Gi/G0 or Gi protein) is a heterotrimeric G protein subunit that inhibits the production of cAMP from ATP.[1] A mnemonic for remembering this subunit is to look at first letter (Gαi = Adenylyl Cyclase inhibitor).

Receptors

The following G protein-coupled receptors couple to the Gi subunit:

Function

Gi mainly inhibits the cAMP dependent pathway by inhibiting adenylate cyclase activity, decreasing the production of cAMP from ATP, which, in turn, results in decreased activity of cAMP-dependent protein kinase. Therefore, the ultimate effect of Gi is the opposite of cAMP-dependent protein kinase.

It is also attributed a minor role in activation of the phospholipase C pathway.[2] Growth hormone is required for normal postnatal growth, bone growth, regulatory effects on protein, carbohydrate, and lipid metabolism.[3] Although this is mainly a function of the Gq alpha subunit.

Types

There are several types of Gi: Gia1, Gia2, Gia3 and Gia4

Gia1

Gia1 or Gi1 is encoded by the gene GNAI1.

Gia2

Gia2 or Gi2 is encoded by the gene GNAI2.

Gia3

Gia3 or Gi3 is encoded by the gene GNAI3.

See also

References

  1. Birnbaumer L (April 2007). "Expansion of signal transduction by G proteins. The second 15 years or so: from 3 to 16 alpha subunits plus betagamma dimers". Biochim. Biophys. Acta. 1768 (4): 772–93. doi:10.1016/j.bbamem.2006.12.002. PMC 1993906. PMID 17258171.
  2. Obál F, Krueger J (2001). "The somatotropic axis and sleep". Rev Neurol (Paris). 157 (11 Pt 2): S12–5. PMID 11924022.
  3. GeneGlobe -> GHRH Signaling[permanent dead link] Retrieved on May 31, 2009

External links