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Difference between revisions of "Peroxisome proliferator-activated receptor gamma coactivator 1-alpha"

From Bioblast
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|abbr=PGC-1α
|abbr=PGC-1α
|description='''Peroxisome proliferator-activated receptor-γ (PPAR-γ) coactivator-1α''' (PGC-1α) is a protein which functions as an inducible transcriptional coactivator, a coregulator of transcription factors, particularly [[NRF-1]] and [[TFAM]]. PGC-1α was first described in 1998 ([[Puigserver_1998_Cell]]). PGC-1α drives the formation of slow-twich muscle fibres ([[Lin_2002_Nature]]) and is increased upon endurance training ([[Norrbom_2004_J Appl Physiol]]). PGC-1α expression is inhibited by the proinflammatory cytokine tumor necrosis factor α (TNF-α) and high levels of leptin. Upregulation of PGC-1α expression is induced by increased [[eNOS]] activity -> [[NO]] -> [[guanylate cyclase]] -> [[cGMP]] ([[Nisoli_2007_Circ Res]]). AMP-activated protein kinase (AMPK) increases PGC-1α expression through SIRT1 ([[Canto_2009_Nature]]).
|description='''Peroxisome proliferator-activated receptor-γ (PPAR-γ) coactivator-1α''' (PGC-1α) is a protein which functions as an inducible transcriptional coactivator, a coregulator of transcription factors, particularly [[NRF-1]] and [[TFAM]]. PGC-1α was first described in 1998 ([[Puigserver_1998_Cell]]). PGC-1α drives the formation of slow-twich muscle fibres ([[Lin_2002_Nature]]) and is increased upon endurance training ([[Norrbom_2004_J Appl Physiol]]). PGC-1α expression is inhibited by the proinflammatory cytokine tumor necrosis factor α (TNF-α) and high levels of leptin. Upregulation of PGC-1α expression is induced by increased [[eNOS]] activity -> [[NO]] -> [[guanylate cyclase]] -> [[cGMP]] ([[Nisoli_2007_Circ Res]]). AMP-activated protein kinase (AMPK) increases PGC-1α expression through SIRT1 ([[Canto_2009_Nature]]).
|info=[http://www.ncbi.nlm.nih.gov/pubmed/20933024 Scarpulla_2011_Biochim Biophys Acta]; [http://www.ncbi.nlm.nih.gov/pubmed/16054085 Lin_2005_Cell Metab]
}}
}}
{{MitoPedia methods}}
{{MitoPedia methods}}
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== Mechanism ==
== Mechanism ==
By interacting with transcription factors, a transcription coactivator, increases the probability of a gene being transcribed without itself binding to DNA in a sequence-specific manner. Although members of the PGC-1 family lack histone acetyltransferase (HAT) activities, their amino-terminal region interacts with proteins containing HAT activity. The HAT activity of this complex remodels histones within chromatin, leading to enzymatic modification of chromatin, increased access of the RNA polymerase II machinery to RNA, thereby activating target gene transcription.
By interacting with transcription factors, a transcription coactivator, increases the probability of a gene being transcribed without itself binding to DNA in a sequence-specific manner. Although members of the PGC-1 family lack histone acetyltransferase (HAT) activities, their amino-terminal region interacts with proteins containing HAT activity. The HAT activity of this complex remodels histones within chromatin, leading to enzymatic modification of chromatin, increased access of the RNA polymerase II machinery to RNA, thereby activating target gene transcription.
== References ==
# [[Canto_2009_Nature]]
# [[Lin_2002_Nature]]
# [http://www.ncbi.nlm.nih.gov/pubmed/16054085 Lin_2005_Cell Metab]
# [[Nisoli_2007_Circ Res]]
# [[Norrbom_2004_J Appl Physiol]]
# [[Puigserver_1998_Cell]]
# [http://www.ncbi.nlm.nih.gov/pubmed/20933024 Scarpulla_2011_Biochim Biophys Acta]

Revision as of 20:57, 4 June 2012


high-resolution terminology - matching measurements at high-resolution


Peroxisome proliferator-activated receptor gamma coactivator 1-alpha

Description

Peroxisome proliferator-activated receptor-γ (PPAR-γ) coactivator-1α (PGC-1α) is a protein which functions as an inducible transcriptional coactivator, a coregulator of transcription factors, particularly NRF-1 and TFAM. PGC-1α was first described in 1998 (Puigserver_1998_Cell). PGC-1α drives the formation of slow-twich muscle fibres (Lin_2002_Nature) and is increased upon endurance training (Norrbom_2004_J Appl Physiol). PGC-1α expression is inhibited by the proinflammatory cytokine tumor necrosis factor α (TNF-α) and high levels of leptin. Upregulation of PGC-1α expression is induced by increased eNOS activity -> NO -> guanylate cyclase -> cGMP (Nisoli_2007_Circ Res). AMP-activated protein kinase (AMPK) increases PGC-1α expression through SIRT1 (Canto_2009_Nature).

Abbreviation: PGC-1α




  • MitoPedia topic: Genetics - Coactivator

PGC-1α

PGC-1α is a member of the PGC-1 family of coactivators, which includes PGC-1β and PGC-1–related coactivator(PRC). PGC-1α is to be a powerful regulator of energy metabolism under conditions of both health and disease and as such interacts with a broad range of transcription factors that are involved in a wide variety of biological responses including adaptive thermogenesis, mitochondrial biogenesis, glucose and fatty acid metabolism, fiber type switching in skeletal muscle, and heart ontogenesis. In general, PGC-1α is highly expressed in mitochondria-rich tissues with active oxidative metabolism such as brown adipose tissue (BAT), the heart, and skeletal muscle.

Mechanism

By interacting with transcription factors, a transcription coactivator, increases the probability of a gene being transcribed without itself binding to DNA in a sequence-specific manner. Although members of the PGC-1 family lack histone acetyltransferase (HAT) activities, their amino-terminal region interacts with proteins containing HAT activity. The HAT activity of this complex remodels histones within chromatin, leading to enzymatic modification of chromatin, increased access of the RNA polymerase II machinery to RNA, thereby activating target gene transcription.

References

  1. Canto_2009_Nature
  2. Lin_2002_Nature
  3. Lin_2005_Cell Metab
  4. Nisoli_2007_Circ Res
  5. Norrbom_2004_J Appl Physiol
  6. Puigserver_1998_Cell
  7. Scarpulla_2011_Biochim Biophys Acta