Any feedback?
Please rate this page
(literature.php)
(0/150)

BRENDA support

Literature summary for 3.4.22.B75 extracted from

  • Karami, S.; Lin, F.M.; Kumar, S.; Bahnassy, S.; Thangavel, H.; Quttina, M.; Li, Y.; Ren, J.; Bawa-Khalfe, T.
    Novel SUMO-protease SENP7S regulates beta-catenin signaling and mammary epithelial cell transformation (2017), Sci. Rep., 7, 46477 .
    View publication on PubMedView publication on EuropePMC
Search for more literature for 3.4.22.B75

Application

Application Comment Organism
medicine SENP7S is the predominant SENP transcript in human mammary epithelia but is significantly reduced in precancerous ductal carcinoma in situ and all breast cancer subtypes Homo sapiens

Localization

Localization Comment Organism GeneOntology No. Textmining
cytosol transcript Senp7S Homo sapiens 5829
-

Organism

Organism UniProt Comment Textmining
Homo sapiens Q9BQF6
-
-

Source Tissue

Source Tissue Comment Organism Textmining
MCF-10-2A cell
-
 Homo sapiens
-
MCF-7 cell
-
 Homo sapiens
-

Substrates and Products (Substrate)

Substrates Comment Substrates Organism Products Comment (Products) Rev. Reac.
axin1 + H2O
-
 Homo sapiens ?
-
 ?
SUMOylated beta-catenin + H2O
-
 Homo sapiens ?
-
 ?

Expression

Organism Comment Expression
Homo sapiens SENP7S is the predominant SENP transcript in human mammary epithelia but is significantly reduced in precancerous ductal carcinoma in situ and all breast cancer subtypes. Like other SENP family members, SENP7S has SUMO isopeptidase activity but unlike full-length SENP7L, SENP7S is localized in the cytosol additional information

General Information

General Information Comment Organism
physiological function SUMOylated beta-catenin and Axin1 are both isoform SENP7S-substrates. With knockdown of SENP7S in mammary epithelial cells, Axin1-beta-catenin interaction is lost and beta-catenin escapes ubiquitylation-dependent proteasomal degradation. SUMOylated beta-catenin accumulates at the chromatin and activates multiple oncogenes. Nontumorigenic MCF10-2A cells with reduced SENP7S exhibit greater cell proliferation and anchorage-dependent growth. SENP7S depletion directly potentiates tumorigenic properties of MCF10-2A cells with induction of anchorage-independent growth and self-renewal in 3D-spheroid conditions Homo sapiens