IndraLab

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"We confirmed that Jab1 over-expression induces the nuclear to cytoplasm translocation of p27 but, to our surprise, treating cells with a p8 siRNA blocked that effect almost completely, indicating that[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

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"Recent studies have demonstrated that jab1 contributes to carcinoma progression by degrading p27 and Kip1 protein."

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"Jun activation domain binding protein 1 negatively regulate p27 kip1 in non Hodgkin 's lymphomas."

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"Jab1 and CSN5 mediated degradation of p27 appears to be a critical mechanism of regulation for this cell cycle inhibitor."

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"RIG-G interacts with JAB1, thus resulting in JAB1 sequestration in the cytoplasm, disturbing the JAB1 normal function, interfering the JAB1 mediated p27 degradation, maintaining p27 protein stability so as to prevent cells from entering the cycle and inhibiting cell proliferation."

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"In Pan et al 's study, 16 Jab1 was found to interact directly with p27 and mediate p27 degradation in a proteasome dependent manner, and high Jab1 expression was found to be associated with poor prognosis in patients with nasopharyngeal carcinoma."

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"Other Jab1 and CSN5 interactions also act to enhance or inhibit Jab1 and CSN5 mediated p27 degradation and are listed in Table XREF_TABLE."

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"So our data suggest that BRSK1 may be a novel tumor suppressor in breast cancer which inversely associated with Jab1 and restored Jab1 induced suppression of p27 Kip1 stability.The current study inves[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

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"Nuclear cytoplasmic translocation plays an important role because leptomycin B (LMB), a chemical inhibitor of CRM1 dependent nuclear export, prevents p27 degradation mediated by Jab1 and CSN5."

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"Our immunohistochemical staining results demonstrated that Jab1 expression was inversely correlated to p27 Kip1 protein expression (P < 0.01), which is consistent with previous results demonstrating that Jab1 negatively regulates p27 in nasopharyngeal carcinoma."

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"As Jab1 can promote the degradation of p27 [XREF_BIBR] and p53 [XREF_BIBR], we further explored the effect of T83 on these two proteins."

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"Indeed, ectopic expression of IFIT3 in U937 human myeloid cells resulted in the sequestration of JUN activation domain-binding protein 1 (JAB1; also known as COPS5), which limited ubiquitin- and proteasome-dependent degradation of cyclin-dependent kinase inhibitor 1B (also known as p27 and KIP1)."

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"Previous studies demonstrated that CSN5 promotes the degradation of p27 Kip1 through the proteasome dependent pathway."

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"Jab1 promotes cell proliferation and inactivates P27 by inducing translocation of P27 from the nucleus to the cytoplasm, which accelerates P27 degradation through the Ub-dependent proteasome pathway and promotes cell cycle progression [ xref ]."

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"Jab1 has been implicated in modulating MIF signaling and conversely, it is also known that MIF abrogates Jab1 mediated degradation of p27 Kip1 [25]."

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"Overexpression of Jab1 reversed the elevated p27 (Kip1) in the nucleus, which needed phosphorylation of p27 (Kip1) on Serine 10, whereas inhibition of Jab1 by siRNA further increased the elevated p27 (Kip1)."

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"These findings suggest that JAB1 overexpression is involved in the pathogenesis of pancreatic cancer through JAB1 mediated p27 degradation and that control of JAB1 expression is a novel therapeutic target in patients with pancreatic adenocarcinomas."

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"Genetic alterations have been reported in NPC, and our recent findings showed that Jab1 and CSN5 is overexpressed and negatively regulates p27 in NPC XREF_BIBR and contribute to radiotherapy and chemotherapy resistance XREF_BIBR, XREF_BIBR."

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"Second, in a manner independent of the CSN holocomplex, CSN5 (or a CSN5 containing small complex) promotes cell proliferation by inducing p27 degradation [22,23] and HIF1-alpha stabilization [41]."

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"JAB1 triggers the proteolytic degradation of p27 XREF_BIBR."

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"BRSK1 expression is inversely correlated with Jab1 and Ki-67 expressions, which may involve in restoring Jab1 induced suppression of p27 Kip1 stability and may regulate cell cycle progression through [MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

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"Gfer inhibits Jab1 mediated degradation of p27kip1 to restrict proliferation of hematopoietic stem cells."

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"Overexpression of JAB1 is found to reduce the half-life of p27Kip1 from more than 5 h to 1.4 h [34], and increase the degradation rate of rLHR by 3 fold [45]."

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"Jab1 promotes p27 degradation through proteolysis and is sensitive to proteasome inhibitors."

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"BRSK1 is a novel tumor suppressor in breast cancer which inversely correlated with Jab1 expression, may involve in the restoring Jab1 induced suppression of p27 (Kip1) and may regulate cell cycle through the PI3K and Akt pathway."

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"One mechanism may involve JAB1 mediated p27 KIP1 degradation [73]."

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"Jab1 and CSN5 negatively regulates p27 and plays a role in the pathogenesis of nasopharyngeal carcinoma."

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"Mechanistically, Jab1 and p27 were found to interact directly in NPC cells, with Jab1 mediating p27 degradation in a proteasome dependent manner."

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"In this study, we identified the role of Jab1 mediated p27 degradation in NPC oncogenesis."

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"Together, our findings suggest that Jab1 overexpression plays an important role in the pathogenesis of NPC through Jab1 mediated p27 degradation."

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"Taken together, our data suggest that CSN5 is necessary for down-regulation of p27 Kip1 by XLGalpha olf, which occurs by mechanisms differing from those reported previously.Next, we screened for poten[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

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"Knockdown of Erv1/ALR in hematopoietic stem cells leads to an increased inhibition of the cyclin-dependent kinase inhibitor p27(kip) by JAB1 while overexpression of ALR leads to a decreased inhibition of p27(kip), probably because JAB1 is sequestered by ALR [ xref ]."

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"As CSN5 is also known to promote the degradation of several proteins, e.g. p53, IkappaBalpha, or p27 [24,25,37], we asked if CSN5 might also affect the degradation of SIAH-1."

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"P27 is a prominent regulator of cell proliferation by universally inhibiting the cell cycle, while Jun activation domain binding protein 1 (Jab1), a multifunctional cell signaling protein, contributes to carcinoma progression by degrading p27."

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"Knockdown of Erv1 and ALR in hematopoietic stem cells leads to an increased inhibition of the cyclin dependent kinase inhibitor p27 (kip) by JAB1 while overexpression of ALR leads to a decreased inhibition of p27 (kip), probably because JAB1 is sequestered by ALR [XREF_BIBR]."

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"By inhibiting Jun activation domain binding protein 1 (Jab1) trastuzumab increases nuclear retention of p27Kip1."

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"Recent studies have demonstrated that jab1 contributes to carcinoma progression by degrading p27 and Kip1 protein."

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"Downregulation of p27 mediated by Jab1 overexpression was inhibited in cells that had been treated with proteasome inhibitors (LLnL, MG132 and LLM) but not in those treated with DMSO (XREF_FIG), indicating that Jab1 promotes p27 degradation through proteolysis and is sensitive to proteasome inhibitors."

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"MIF signals through at least three cell surface receptors, including the CD74/44 complex, CXCR2 and CXCR4 16-18 but also signals by intracellular interaction with the JAB-1 thus inhibiting JNK activation and p27 Kip1 -dependent cell-cycle regulation."

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"In addition, we recently found that Jab1 and CSN5 promotes p27 degradation via proteolysis."

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"Jab1 promotes degradation of the cyclin dependent kinase inhibitor p27 (Kip1) by transportation from the nucleus to the cytoplasm."

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"Next, we confirmed the down-regulation of p27 Kip1 by CSN5, but unexpectedly, overexpression of CSN5 did not change the expression of p27 Kip1 in HEK-293FT cells (data not shown)."

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"Since previous reports showed that CSN5 promotes degradation of p27 Kip1 in a proteasome dependent manner, MG132 was added to the culture medium to analyze whether this pathway was responsible for the[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

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"The findings suggest that Jab1 overexpression plays an important role in the pathogenesis of NPC through Jab1 mediated p27 degradation."

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"Specifically, the Jab1 subunit of the COP9 complex is reported to modulate the degradation of p27 protein (Tomoda et al., 1999)."

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"A Jab1 and CSN5 truncation mutant lacking NES reversed p27 down-regulation induced by the full-length Jab1 and CSN5, indicating that this mutant functions as a dominant negative (DN-Jab1)."

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"These findings suggest that Jab1 protein may contribute to the tumor progression through Jab1 mediated p27kip1 degradation and that control of Jab1 expression is a novel therapeutic target with NHLs."

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"Jab1, a co-activator of AP-1 transcription factor and the fifth subunit of the COP9 signalosome, mediates degradation of the tumor suppressor p53 and p27 (Kip1) and functions as a tumor promoter in different types of human cancer."