Literature summary for 1.14.11.7 extracted from

Liu, Y.; Huo, Z.; Yan, B.; Lin, X.; Zhou, Z.N.; Liang, X.; Zhu, W.; Liang, D.; Li, L.; Liu, Y.; Zhao, H.; Sun, Y.; Chen, Y.H.
Prolyl hydroxylase 3 interacts with Bcl-2 to regulate doxorubicin-induced apoptosis in H9c2 cells (2010), Biochem. Biophys. Res. Commun., 401, 231-237.

Search for more literature for 1.14.11.7

Organism

Organism	UniProt	Comment	Textmining
Rattus norvegicus	-	-	-

Source Tissue

Source Tissue	Comment	Organism	Textmining
H9c2 cell	a cell line with myogenic potential derived from embryonic rat heart	Rattus norvegicus	-

Substrates and Products (Substrate)

Substrates	Comment Substrates	Organism	Products	Comment (Products)	Rev.	Reac.
additional information	the BH4 domain is required for the interaction of PHD3 with Bcl-2, PHD3 promotes apoptosis via its BH4 domain	Rattus norvegicus	?	-	?

Synonyms

Synonyms	Comment	Organism
PHD3	-	Rattus norvegicus
prolyl hydroxylase	-	Rattus norvegicus

Expression

Organism	Comment	Expression
Rattus norvegicus	after apoptosis of H9c2 cells is induced by DOX, PHD3 expression is upregulated in a time-dependent manner, whereas the expression of PHD1 or PHD2 is constant	up

General Information

General Information	Comment	Organism
additional information	PHD3 upregulation contributes to doxorubicin-induced apoptosis in H9c2 cells. Overexpression of PHD3 counteracts the formation of the BaxBcl-2 complex, the BH4 domain of anti-apoptosis protein Bcl-2 is required for its interaction with PHD3. BaxBcl-2 complex formation is significantly reduced in apoptotic H9c2 cells in which PHD3 is overexpressed compared to the apoptotic H9c2 cells with native PHD3 levels	Rattus norvegicus
physiological function	role of PHD3 in the apoptosis of cardiac myocytes. PHD3 promotes the apoptosis of H9c2 cells via an interaction with the BH4 domain of Bcl-2, it affects the formation of the BaxBcl-2 complex	Rattus norvegicus

Use of this online version of BRENDA is free under the CC BY 4.0 license. See terms of use for full details.

Release 2023.1 (January 2023)