IndraLab

Statements



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"Likewise, Sang et al. have reported that inhibition of Jab1 and COPS5 promoted the apoptosis through p53 related apoptotic pathways in gastric cancer cells."

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"Mechanistic investigation revealed that CSN5i-3 inhibited Jab1 expression and increased the expression of apoptosis marker cleaved caspase3 and cell cycle related protein p27 in BT474 and SKBR3 cells."

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"Suppression of CSN5 promotes the apoptosis of gastric cancer cells through regulating p53 related apoptotic pathways."

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"Several targets of Jab1 and CSN5, including p27, p53, c-myc, and cyclin E, were found to be highly expressed in Jab1 and CSN5 -/- embryos, resulting in impaired proliferation and accelerated apoptosis [XREF_BIBR, XREF_BIBR]."

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"However, there was no significant difference between the control and Jab1-siRNA treated groups; thus, we can not conclude that Jab1 knockdown initiates apoptosis under these conditions."

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"(Phospho)-beta-catenin levels were found to be reduced following CSN5 knockdown and CSN5 promoted CRC cell proliferation but also apoptosis [30]."

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"Jab1 and COPS5 knockdown significantly inhibits proliferation and induces apoptosis in hepatocellular carcinoma cells."

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"This data complements previous studies demonstrating that CSN5 loss inhibits proliferation and induces apoptosis [XREF_BIBR - XREF_BIBR]."

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"XREF_BIBR used T83 (a new 4-arylidene curcumin analogue) to inhibit the expression of Jab1 in NPC cells, demonstrating that inhibition of Jab1 could reduce tumor cell growth, induce G 2 / M arrest, and increase tumor cell apoptosis, thus enhancing the sensitivities of NPC cells to radiotherapy."

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"Conditional deletion of Jab1 and CSN5 in thymocytes resulted in defective S-phase progression and increased apoptosis that could be attributed to CSN substrates, including p53, IkappaB-alpha, and beta-catenin."

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"Jab1 and CSN5 knockdown also impaired proliferation and enhanced apoptosis in these cells regardless of the genotype of the tumor suppressor p53 [XREF_BIBR]."

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"The constitutive deletion of Jab1 in mice results in early embryonic lethality by E8.5, with impaired proliferation and accelerated apoptosis, thus underscoring the essential role of Jab1 in overall early embryogenesis."

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"Suppression of Jab1 expression inhibits proliferation and promotes apoptosis of AMC-HN-8 cells."

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"Loss of Jab1 sensitized cells to gamma radiation induced apoptosis and increased spontaneous DNA damage and homologous recombination defects."

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"Jab1 and CSN5 inhibits cisplatin- and radiation- induced apoptosis of NPC cells."

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"Positive staining using the TUNEL assay confirmed that loss of CSN5 could induce germ cell apoptosis."

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"Our results showed that knockdown of CSN5 could inhibit proliferation and promote apoptosis of gastric cancer cells."

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"Indeed, the constitutive deletion of Jab1 in mice results in early embryonic lethality by E8.5 with impaired proliferation and increased apoptosis (Tian et al., 2010; Tomoda, Yoneda-Kato, Fukumoto, Yamanaka, & Kato, 2004)."

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"Thus, in our next experiments we determined whether loss of Jab1 promotes apoptosis of NPC cells in response to DNA damage."

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"The knockdown of JAB1 impairs cell cycle progression , increases apoptosis , and its overexpression in human osteosarcoma is correlated with poor prognosis ."

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"Moreover, silencing Jab1 protein expression declined tumor growth and further increased the apoptosis rate of gastric cancer cells."

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"Silencing CSN5 triggers cancer cell apoptosis with significant up-regulation of p53 protein [XREF_BIBR, XREF_BIBR]."

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"By contrast, overexpression of Jab1 in CNE1 cells blocked cisplatin- and UV radiation induced apoptosis, as measured by Hoechst 33342 staining and analysis of PARP and caspase-3 cleavage."