IndraLab

Statements



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"Knockdown of either CSN2 or CSN5 dramatically diminished cell proliferation, followed by loss of cell viability."

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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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"Because CSN5/Jab1-depletion effectively prevented cell proliferation and survival (see below), and it is reported that conditional knockout of the CSN5/Jab1 gene in mice allowed cells in which CSN5/Ja[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

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"CSN5/Jab1-depletion (CSN5/Jab1 −/f allele + CRE) markedly inhibited cell proliferation, whereas introduction of the CRE recombinase itself had little effect because wild-type MEFs infected with the CR[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

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"Interestingly, siRNA-mediated depletion of Jab1 inhibited cell proliferation and accelerated apoptotic cell death in NPC."

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"The downregulation of HIF1A and COPS5 has been shown to inhibit the proliferation and malignant behaviors of cancer cells, suggesting that inhibitors targeting the two proteins may have potential as anticancer therapeutics ."

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"Knockdown of Jab1 and COPS5 results in the accumulation of p27 in cell nucleus, induces cell-cycle arrest and inhibits cell proliferation."

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"Interestingly, siRNA mediated depletion of Jab1 inhibited cell proliferation and accelerated apoptotic cell death in NPC."

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"In all cells, downregulation of JAB1 inhibited cell proliferation (left panel, Fig. 6 A)."

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"We found that downregulation of CSN5 in Siha and Hela cells inhibited cell proliferation in vitro and in vivo, and the inhibitory effects were largely rescued by CSN5 overexpression."

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"Depletion of Jab1/CSN5 by siRNA increases accumulation of p27 and induces cell-cycle arrest and inhibits cell proliferation ( Pan et al., 2012 )."

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"Knockdown of Jab1 by small interfering RNA (siRNA) preferentially inhibited proliferation of HER-2 and neu-overexpressing breast cancer cells."

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"Further studies revealed that depletion of Jab1 inhibited cell proliferation, and induced premature senescence characterized by upregulation of senescence associated- beta-galactosidase activity and increased expression of CDK inhibitors."

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"In both, Bezielle inhibited cell proliferation, induced cell death and G2 cycle arrest by regulating the mediator proteins Jab1, p27 (Kip1) and p21 (Cip1)."

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"In mammalian cells, knock-down of CSN3 or CSN8 in cultured cells can accelerate cell proliferation [XREF_BIBR, XREF_BIBR], whereas knock-down of CSN5 decreases cell proliferation and causes cell senescence [XREF_BIBR, XREF_BIBR]."

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"Knockdown of CSN5 inhibits the proliferation of human tumor cells XREF_BIBR XREF_BIBR, suggesting that overexpression of CSN5 not only serves as a marker of malignant transformation, but also actually contributes to tumor cell proliferation."

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"The results showed that downregulation of Jab1 significantly inhibited glioma cell proliferation, while overexpression of Jab1 promoted it."

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"Depletion of Jab1 by siRNA increases accumulation of p27 and induces cell-cycle arrest and inhibits cell proliferation in NPC cell lines."