Sterol regulatory element-binding protein 1: Difference between revisions
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== | {{Infobox protein | ||
| name = Sterol regulatory element-binding protein 1 | |||
| image = <!-- Image removed --> | |||
| caption = <!-- Caption removed --> | |||
| symbol = SREBF1 | |||
| alt_symbols = SREBP1 | |||
| EntrezGene = 6720 | |||
| HGNCid = 11283 | |||
| OMIM = 184756 | |||
| RefSeq = NM_004176 | |||
| UniProt = P36956 | |||
}} | |||
'''Sterol regulatory element-binding protein 1''' ('''SREBP1''') is a transcription factor that plays a crucial role in the regulation of [[lipid metabolism]]. It is encoded by the '''SREBF1''' gene in humans. SREBP1 is involved in the synthesis of [[cholesterol]], [[fatty acids]], and [[triglycerides]]. | |||
== Function == | == Function == | ||
SREBP1 is a member of the [[basic helix-loop-helix]] leucine zipper (bHLH-Zip) family of transcription factors. It binds to the sterol regulatory element (SRE) in the promoter region of target genes, activating their transcription. This process is essential for maintaining cellular lipid homeostasis. | |||
SREBP1 exists in two isoforms, SREBP1a and SREBP1c, which are generated by alternative splicing. SREBP1c is primarily involved in the regulation of [[fatty acid synthesis]], while SREBP1a has a broader role, influencing both fatty acid and cholesterol synthesis. | |||
== Regulation == | |||
The activity of SREBP1 is tightly regulated by [[sterol]] levels within the cell. Under low sterol conditions, SREBP1 is transported from the [[endoplasmic reticulum]] to the [[Golgi apparatus]], where it is cleaved by site-1 and site-2 proteases. The cleaved, active form of SREBP1 then translocates to the [[nucleus]] to activate gene expression. | |||
In contrast, high sterol levels inhibit the cleavage and activation of SREBP1, thereby reducing the expression of its target genes and decreasing lipid synthesis. | |||
== | == Clinical Significance == | ||
Dysregulation of SREBP1 activity is associated with various metabolic disorders, including [[obesity]], [[insulin resistance]], and [[non-alcoholic fatty liver disease]] (NAFLD). Overexpression of SREBP1 can lead to excessive lipid accumulation in tissues, contributing to the development of these conditions. | |||
Research into SREBP1 and its regulatory pathways is ongoing, with the aim of developing therapeutic strategies to modulate its activity in metabolic diseases. | |||
== See Also == | == See Also == | ||
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* [[Lipid metabolism]] | * [[Lipid metabolism]] | ||
* [[Transcription factor]] | * [[Transcription factor]] | ||
== References == | == References == | ||
<references /> | <references /> | ||
== External Links == | |||
* [GeneCards: SREBF1](https://www.genecards.org/cgi-bin/carddisp.pl?gene=SREBF1) | |||
* [UniProt: P36956](https://www.uniprot.org/uniprot/P36956) | |||
{{ | |||
{{Protein-stub}} | |||
[[Category:Transcription factors]] | [[Category:Transcription factors]] | ||
[[Category:Lipid metabolism]] | |||
[[Category:Human proteins]] | [[Category:Human proteins]] | ||
Latest revision as of 21:49, 29 December 2024
Sterol regulatory element-binding protein 1 (SREBP1) is a transcription factor that plays a crucial role in the regulation of lipid metabolism. It is encoded by the SREBF1 gene in humans. SREBP1 is involved in the synthesis of cholesterol, fatty acids, and triglycerides.
Function[edit]
SREBP1 is a member of the basic helix-loop-helix leucine zipper (bHLH-Zip) family of transcription factors. It binds to the sterol regulatory element (SRE) in the promoter region of target genes, activating their transcription. This process is essential for maintaining cellular lipid homeostasis.
SREBP1 exists in two isoforms, SREBP1a and SREBP1c, which are generated by alternative splicing. SREBP1c is primarily involved in the regulation of fatty acid synthesis, while SREBP1a has a broader role, influencing both fatty acid and cholesterol synthesis.
Regulation[edit]
The activity of SREBP1 is tightly regulated by sterol levels within the cell. Under low sterol conditions, SREBP1 is transported from the endoplasmic reticulum to the Golgi apparatus, where it is cleaved by site-1 and site-2 proteases. The cleaved, active form of SREBP1 then translocates to the nucleus to activate gene expression.
In contrast, high sterol levels inhibit the cleavage and activation of SREBP1, thereby reducing the expression of its target genes and decreasing lipid synthesis.
Clinical Significance[edit]
Dysregulation of SREBP1 activity is associated with various metabolic disorders, including obesity, insulin resistance, and non-alcoholic fatty liver disease (NAFLD). Overexpression of SREBP1 can lead to excessive lipid accumulation in tissues, contributing to the development of these conditions.
Research into SREBP1 and its regulatory pathways is ongoing, with the aim of developing therapeutic strategies to modulate its activity in metabolic diseases.
See Also[edit]
References[edit]
<references />
External Links[edit]
- [GeneCards: SREBF1](https://www.genecards.org/cgi-bin/carddisp.pl?gene=SREBF1)
- [UniProt: P36956](https://www.uniprot.org/uniprot/P36956)
