RelA/NF-κB transcription factor associates with α-actinin-4

Babakov, Vladimir; Petukhova, Olga; Turoverova, Lidia; Kropacheva, I. V.; Tentler, Dmitri; Bolshakova, Anastasia; Podolskaya, Е. P.; Magnusson, Karl‐Eric; Пинаев, Г. П.

doi:10.1016/j.yexcr.2007.12.001

Cited by 49 publications

(49 citation statements)

References 45 publications

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“…The invasive ability of the mesenchymal ACTN4 KD WM1158 cells through the three-dimensional collagen I matrix was significantly inhibited. The amoeboidal to mesenchymal transition coincided with the loss of RSF and would be consistent with the putative role of ACTN4 in linking the cytoskeleton to the membrane (25,26). This may be why down-regulation of ACTN4 but not ACTN1 impairs the migration of astrocytoma cells (20).…”

Section: Discussionsupporting

confidence: 70%

α-Actinin-4 Is Required for Amoeboid-type Invasiveness of Melanoma Cells

Shao

Watkins

et al. 2014

Journal of Biological Chemistry

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Background: Melanoma cells invasion through the dermis directly correlates with death, defining migration as critical. Results: ACTN4 down-regulation limits aggressive melanoma cells to a mesenchymal phenotype that retards collagen I matrix invasiveness. Conclusion: Amoeboidal morphology necessary for melanoma invasion requires ACTN4. Significance: This finding provides for a role of ACTN4 in melanoma invasion and implicates a linkage between actin cytoskeleton and melanoma progression.

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Section: Discussionsupporting

confidence: 70%

α-Actinin-4 Is Required for Amoeboid-type Invasiveness of Melanoma Cells

Shao

Watkins

et al. 2014

Journal of Biological Chemistry

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“…This nuclear accumulation was also observed in A431 cells treated with tumor necrosis factor (TNF) or epidermal growth factor (EGF) in association with the p65 subunit of nuclear factor (NF)-B. These findings most probably indicate a specific role for actinin-4, as actinin-1 has not been detected in the nucleus to date (Babakov et al, 2008). Several proteins that play an important structural role in the cytoplasm are also localized to the nucleus, including SRcontaining proteins such as the spectrins, nesprins, bullous pemphigoid antigen 1 (Bpag1) and nuclear mitotic apparatus protein (NuMA) (Young and Kothary, 2005).…”

Section: Introductionmentioning

confidence: 87%

Molecular mechanisms underlying nucleocytoplasmic shuttling of actinin-4

Kumeta

Yoshimura

Harata

et al. 2010

Journal of Cell Science

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SummaryIn addition to its well-known role as a crosslinker of actin filaments at focal-adhesion sites, actinin-4 is known to be localized to the nucleus. In this study, we reveal the molecular mechanism underlying nuclear localization of actinin-4 and its novel interactions with transcriptional regulators. We found that actinin-4 is imported into the nucleus through the nuclear pore complex in an importinindependent manner and is exported by the chromosome region maintenance-1 (CRM1)-dependent pathway. Nuclear actinin-4 levels were significantly increased in the late G2 phase of the cell cycle and were decreased in the G1 phase, suggesting that active release from the actin cytoskeleton was responsible for increased nuclear actinin-4 in late G2. Nuclear actinin-4 was found to interact with the INO80 chromatin-remodeling complex. It also directs the expression of a subset of cell-cycle-related genes and interacts with the upstream-binding factor (UBF)-dependent rRNA transcriptional machinery in the M phase. These findings provide molecular mechanisms for both nucleocytoplasmic shuttling of proteins that do not contain a nuclear-localization signal and cell-cycle-dependent gene regulation that reflects morphological changes in the cytoskeleton.

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“…Nuclear translocation of the NF-B family of transcription factors is an essential step to regulate the expression of their target genes. A previous study has suggested that overexpression of ACTN4 promoted nuclear translocation of p65 (26). To further dissect the mechanism by which loss of ACTN4 decreased NF-B reporter activity and its target gene expression, we determined whether knockdown of ACTN4 affects TNF␣-induced nuclear translocation of p65.…”

Section: Actn4 Is Required For Nf-b Transcriptional Activity-ourmentioning

confidence: 99%

α-Actinin 4 Potentiates Nuclear Factor κ-Light-chain-enhancer of Activated B-cell (NF-κB) Activity in Podocytes Independent of Its Cytoplasmic Actin Binding Function

Zhao¹,

Hsu²,

Lim³

et al. 2015

Journal of Biological Chemistry

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Background: ACTN4 is an actin-binding protein and is associated with kidney diseases. Results: Nuclear ACTN4 interacts with NF-B and is recruited to NF-B-targeted promoters to potentiate its transcription activity. Conclusion: ACTN4 coactivates NF-B activity independently of its cytoplasmic activity in cultured human podocytes. Significance: Nuclear ACTN4 may play an important role in glomerular function.

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RelA/NF-κB transcription factor associates with α-actinin-4

Cited by 49 publications

References 45 publications

α-Actinin-4 Is Required for Amoeboid-type Invasiveness of Melanoma Cells

α-Actinin-4 Is Required for Amoeboid-type Invasiveness of Melanoma Cells

Molecular mechanisms underlying nucleocytoplasmic shuttling of actinin-4

α-Actinin 4 Potentiates Nuclear Factor κ-Light-chain-enhancer of Activated B-cell (NF-κB) Activity in Podocytes Independent of Its Cytoplasmic Actin Binding Function

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