ING1a expression increases during replicative senescence and induces a senescent phenotype

Soliman, Mohamed A.; Berardi, Philip; Pastyryeva, Svitlana; Bonnefin, Paul; Feng, Xiaolan; Colina, Ana Rosa; Young, Dallan; Riabowol, Karl

doi:10.1111/j.1474-9726.2008.00427.x

Cited by 54 publications

(80 citation statements)

References 72 publications

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“…As SAHFs are very good markers of senescence, at the moment it is not possible to distinguish if this phenotype is due to direct roles of ING1 proteins in SAHF formation or merely reflect their ability to induce senescence. In a very recent report, Soliman et al have presented evidence of the preferential binding of ING1 proteins to the promoter of the PCNA gene in senescent fibroblasts, by chromatin immunoprecipitation [88]. As indicated, PCNA is one of the loci silenced in SAHFs.…”

Section: Role Of Ing Proteins In Regulation Of Gene Expression and Chmentioning

confidence: 99%

“…Although these results suggest a differential behavior of ING proteins in terms of chromatin binding in senescent fibroblasts, their connection with structures like the SAHFs is not clear. Enforced expression of either p47ING1a [88], or p33ING1b (Abad et al, submitted) in early passage human fibroblasts results in formation of SAHFs. As SAHFs are very good markers of senescence, at the moment it is not possible to distinguish if this phenotype is due to direct roles of ING1 proteins in SAHF formation or merely reflect their ability to induce senescence.…”

Section: Role Of Ing Proteins In Regulation Of Gene Expression and Chmentioning

confidence: 99%

“…However, it should be noted that ING1 proteins were not found in other SAHF-regulated loci, like cyclin A, and thus the generality of this finding remains to be tested. Interestingly, although it was found that expression of PCNA could be repressed by ectopic p47ING1a, the specific contribution of each ING1 isoform was not determined in the chromatin binding assays, opening the possibility for roles for both ING1 isoforms [87,88]. We have also investigated the possible participation of ING1 proteins in SAHFs by immunofluorescence.…”

Section: Role Of Ing Proteins In Regulation Of Gene Expression and Chmentioning

confidence: 99%

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ING Proteins in Cellular Senescence

Menéndez¹,

Abad²,

Gómez-Cabello³

et al. 2009

CDT

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Cellular senescence is an effective anti-tumor barrier that acts by restraining the uncontrolled proliferation of cells carrying potentially oncogenic alterations. ING proteins are putative tumor suppressor proteins functionally linked to the p53 pathway and to chromatin regulation. ING proteins exert their tumor-protective action through different types of responses. Here, we review the evidence on the participation of ING proteins, mainly ING1 and ING2, in the implementation of the senescent response. The currently available data support an important role of ING proteins as regulators of senescence, in connection with the p53 pathway and chromatin organization.

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Section: Role Of Ing Proteins In Regulation Of Gene Expression and Chmentioning

confidence: 99%

Section: Role Of Ing Proteins In Regulation Of Gene Expression and Chmentioning

confidence: 99%

Section: Role Of Ing Proteins In Regulation Of Gene Expression and Chmentioning

confidence: 99%

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ING Proteins in Cellular Senescence

Menéndez¹,

Abad²,

Gómez-Cabello³

et al. 2009

CDT

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“…Since ING1 isoforms are differentially expressed during cellular senescence [41] upregulates ING2a protein level in a ligand-dependent manner (Fig. 4b).…”

Section: Ing1b Regulates the Stability Of Ing2a Proteinmentioning

confidence: 99%

A novel crosstalk between the tumor suppressors ING1 and ING2 regulates androgen receptor signaling

et al. 2016

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“…Senescent cells also mislocalize a number of proteins such as actin and lamin A. The basis for mislocalization of proteins is unknown, but it may be a function of alternative isoforms being expressed (Cao et al 2011 ;Soliman et al 2008 ).…”

Section: Morphological Changesmentioning

confidence: 99%

Function of the ING Proteins in Cancer and Senescence

Tran

Rajarajacholan

Riabowol

2013

Tumor Dormancy, Quiescence, and Senescence, Volume 2

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Age is one of the strongest correlates to the incidence of cancers known, suggesting that the two processes are linked. Cell aging (senescence) is increasingly being linked to epigenetic pathways, many of which have recently been found to be markedly altered in precancerous and cancer cells. Thus, misregulation of epigenetic pathways may impact both cancer and aging by infl uencing genetic and biochemical pathways common to both processes. Similar to the p53 and retinoblastoma (Rb) tumor suppressors that affect chromatin structure by genetic and epigenetic mechanisms, the IN hibitor of G rowth (ING) type II tumour suppressors affect pathways that contribute to cell aging and cancer. In particular, the INGs have been demonstrated to act as readers of the histone code by virtue of interacting specifi cally with the histone H3 residue H3K4Me3 and as targeting subunits of the writers of the histone code by being stoichiometric members of histone acetyltransferase (HAT) and histone deacetylase (HDAC) complexes. The ING proteins are frequently

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ING1a expression increases during replicative senescence and induces a senescent phenotype

Cited by 54 publications

References 72 publications

ING Proteins in Cellular Senescence

ING Proteins in Cellular Senescence

A novel crosstalk between the tumor suppressors ING1 and ING2 regulates androgen receptor signaling

Function of the ING Proteins in Cancer and Senescence

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