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TMCO1 (zeige TMCO1 Proteine) recruited the PH domain and leucine-rich repeat protein phosphatase 2 (PHLPP2) to dephosphorylate pAKT1(serine 473) (S473). Mutagenesis at S60 of the TMCO1 (zeige TMCO1 Proteine) protein released TMCO1 (zeige TMCO1 Proteine)-induced cell-cycle arrest and restored the AKT (zeige AKT1 Proteine) pathway in BFTC905 cells. Stable TMCO1 (zeige TMCO1 Proteine) (wild-type) overexpression suppressed, whereas T33A and S60A mutants recovered, tumor size in xenograft mice.
Cheliensisin A (Chel A)treatment led to PH domain and Leucine rich repeat Protein (zeige NYX Proteine) Phosphatases (PHLPP2) protein degradation and subsequently increased in c-Jun (zeige JUN Proteine) phosphorylation, which could be attenuated by inhibition of autophagy mediated by Beclin 1 (zeige BECN1 Proteine).
Results show that MiR (zeige MLXIP Proteine)-27a directly targets PHLPP2 by binding to its 3'-UTR to inhibit its expression, and that downregulation of PHLPP2 could rescue the effect of anti-miR (zeige MLXIP Proteine)-27a in gastric cancer cells.
miR (zeige MLXIP Proteine)-938 promoted CRC (zeige CALR Proteine) cell proliferation by inhibiting PHLPP2
two PHLPP isozymes, PHLPP1 and PHLPP2, were identified in a search for phosphatases that dephosphorylate Akt (zeige AKT1 Proteine), and thus suppress growth factor signaling.
results identify a novel role of PHLPP in regulating aPKC and cell polarity.
Low PHLPP2 expression is associated with luminal breast cancer.
miR (zeige MLXIP Proteine)-3117 contributes to the proliferation of HepG2 by targeting PHLPPL.
Overexpression of PHLPP2 without its 3'UTR attenuated the effects of miR (zeige MLXIP Proteine)-181a on cell proliferation and apoptosis in keloid fibroblast cells.
Suggest that direct PHLPP2 downregulation is required for miR (zeige MLXIP Proteine)-32-induced cell proliferation of breast cancer cells.
KCTD17, which is up-regulated in liver tissues of obese mice and patients with NAFLD, binds to phosphorylated PHLPP2 to target it for ubiquitin-mediated degradation; this increases expression of genes that regulate lipogenesis to promote hepatic steatosis.
PHLPP is a negative regulator of RAF1 (zeige RAF1 Proteine), which reduces colorectal cancer cell motility and prevents tumor progression in mice.
Protein phosphatase that mediates dephosphorylation of 'Ser-473' of AKT1, 'Ser-660' of PRKCB isoform beta-II and 'Ser- 657' of PRKCA. AKT1 regulates the balance between cell survival and apoptosis through a cascade that primarily alters the function of transcription factors that regulate pro- and antiapoptotic genes. Dephosphorylation of 'Ser-473' of AKT1 triggers apoptosis and decreases cell proliferation. Also controls the phosphorylation of AKT3. Dephosphorylation of PRKCA and PRKCB leads to their destabilization and degradation. Inhibits cancer cell proliferation and may act as a tumor suppressor.
PH domain leucine-rich repeat-containing protein phosphatase 2
, PH domain and leucine rich repeat protein phosphatase 2
, PH domain leucine-rich repeat-containing protein phosphatase 2-like
, GTPase activating protein and VPS9 domains 1