PIAS1,2-1 SUMOylate HIC1 with SUMO1

Stable Identifier
Reaction [transition]
Homo sapiens
Locations in the PathwayBrowser
SVG |   | PPTX  | SBGN
Click the image above or here to open this reaction in the Pathway Browser
The layout of this reaction may differ from that in the pathway view due to the constraints in pathway layout
PIAS1,2-1 SUMOylate deacetylated HIC1 at lysine-333 (lysine 314 of HIC1 isoform 2) with SUMO1 (Stankovic-Valentin et al. 2007). Acetylation of HIC1 at lysine-333 inhibits SUMOylation. SUMOylation increases transcription repression by HIC1 (Stankovic-Valentin et al. 2007) and favors the interaction of HIC1 with MTA1 (Van Rechem et al., Mol Cell Biol, 2010) and MTA3 (Paget et al. 2016) notably during the DNA damage response (DDR) to non-repairable double strand breaks (DSBs).(Dehennaut et al. 2013). This increase of HIC1 SUMOylation during the DDR to DSBs is strictly dependent on the ATM kinase (Paget et al. 2016). SUMOylation of HIC1 is dispensable for DNA repair since the non-SUMOylatable point mutant E316A is as efficient as wt HIC1 in Comet assays which measure the repair of DSBs (Paget et al. 2016).
Literature References
PubMed ID Title Journal Year
23417673 DNA double-strand breaks lead to activation of hypermethylated in cancer 1 (HIC1) by SUMOylation to regulate DNA repair

Abbadie, C, Nassour, J, Leprince, D, Dehennaut, V, Dubuissez, M, Loison, I

J. Biol. Chem. 2013
17283066 An acetylation/deacetylation-SUMOylation switch through a phylogenetically conserved psiKXEP motif in the tumor suppressor HIC1 regulates transcriptional repression activity

Vergoten, G, Dejean, A, Pinte, S, Seeler, J, Deltour, S, Stankovic-Valentin, N, Leprince, D, Guérardel, C

Mol. Cell. Biol. 2007
20547755 Differential regulation of HIC1 target genes by CtBP and NuRD, via an acetylation/SUMOylation switch, in quiescent versus proliferating cells

Boulay, G, Pinte, S, Van Rechem, C, Stankovic-Valentin, N, Leprince, D, Guérardel, C

Mol. Cell. Biol. 2010
27935866 HIC1 (hypermethylated in cancer 1) SUMOylation is dispensable for DNA repair but is essential for the apoptotic DNA damage response (DDR) to irreparable DNA double-strand breaks (DSBs)

Abbadie, C, Spruyt, N, Nassour, J, Paget, S, Rood, BR, Leprince, D, Harmon, BT, Dehennaut, V, Loison, I, Dubuissez, M

Oncotarget 2016
Catalyst Activity

SUMO transferase activity of PIAS1,2-1 [nucleoplasm]

Orthologous Events
Cite Us!