CEBPD: Difference between revisions
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'''CEBPD''' or '''CCAAT/enhancer-binding protein delta''' is a [[protein]] that in humans is encoded by the ''CEBPD'' [[gene]]. This protein is a member of the [[CCAAT/enhancer-binding protein]] (C/EBP) family of [[transcription factors]]. | '''CEBPD''' or '''CCAAT/enhancer-binding protein delta''' is a [[protein]] that in humans is encoded by the ''CEBPD'' [[gene]]. This protein is a member of the [[CCAAT/enhancer-binding protein]] (C/EBP) family of [[transcription factors]]. | ||
[[File:1gtw.png|thumb|right|300px|The CEBPD protein.]] | |||
== Function == | == Function == | ||
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Mutations in the ''CEBPD'' gene have been associated with various diseases, including [[cancer]], [[diabetes]], and [[inflammatory diseases]]. The protein's role in apoptosis and inflammatory response also makes it a potential target for drug development. | Mutations in the ''CEBPD'' gene have been associated with various diseases, including [[cancer]], [[diabetes]], and [[inflammatory diseases]]. The protein's role in apoptosis and inflammatory response also makes it a potential target for drug development. | ||
== See also == | == See also == | ||
Latest revision as of 15:04, 12 July 2024
CEBPD or CCAAT/enhancer-binding protein delta is a protein that in humans is encoded by the CEBPD gene. This protein is a member of the CCAAT/enhancer-binding protein (C/EBP) family of transcription factors.
Function[edit]
The protein functions as a dominant-negative inhibitor by forming heterodimers with other C/EBP members, such as C/EBP and liver activator protein (LAP), and preventing their DNA binding activity. The protein is implicated in adipogenesis and erythropoiesis, is activated by endoplasmic reticulum stress, and promotes apoptosis.
Clinical significance[edit]
Mutations in the CEBPD gene have been associated with various diseases, including cancer, diabetes, and inflammatory diseases. The protein's role in apoptosis and inflammatory response also makes it a potential target for drug development.
See also[edit]
References[edit]
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