The interferon-inducible p200 family of proteins: a perspective on their roles in cell cycle regulation and differentiation

Asefa, Benyam

doi:10.1016/j.bcmd.2003.10.002

Cited by 123 publications

(109 citation statements)

References 92 publications

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“…Recent data suggest that there is a strong correlation between MNDA expression and myeloid differentiation. 56 Here, MNDA expression further elucidates the myeloid lineage specificity in t(11q23)/MLL-positive AML. Lastly, CITED4, a CBP/p300-interacting transcriptional transactivator, is significantly higher expressed in AML with t(11q23)/MLL.…”

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confidence: 79%

New insights into MLL gene rearranged acute leukemias using gene expression profiling: shared pathways, lineage commitment, and partner genes

et al. 2005

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Rearrangements of the MLL gene occur in both acute lymphoblastic and acute myeloid leukemias (ALL, AML). This study addressed the global gene expression pattern of these two leukemia subtypes with respect to common deregulated pathways and lineage-associated differences. We analyzed 73 t(11q23)/MLL leukemias in comparison to 290 other acute leukemias and demonstrate that 11q23 leukemias combined are characterized by a common specific gene expression signature. Additionally, in unsupervised and supervised data analysis algorithms, ALL and AML cases with t(11q23) segregate according to the lineage they are derived from, that is, myeloid or lymphoid, respectively. This segregation can be explained by a highly differing transcriptional program. Through the use of novel biological network analyses, essential regulators of early B cell development, PAX5 and EBF, were shown to be associated with a clear B-lineage commitment in lymphoblastic t(11q23)/MLL leukemias. Also, the influence of the different MLL translocation partners on the transcriptional program was directly assessed. Interestingly, gene expression profiling did not reveal a clear distinct pattern associated with one of the analyzed partner genes. Taken together, the identified molecular expression pattern of MLL fusion gene samples and biological networks revealed new insights into the aberrant transcriptional program in 11q23/MLL leukemias. Leukemia (2005) 19, 953-964.

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confidence: 79%

New insights into MLL gene rearranged acute leukemias using gene expression profiling: shared pathways, lineage commitment, and partner genes

et al. 2005

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“…IFI16 is one of the few IFN-inducible genes directly involved in the regulation of cell proliferation and differentiation (61). There is increasing evidence that members of the IFI p200 family (including IFI16) may be regulated by stimuli, independent of the IFNs (59,61,62).…”

Section: Discussionmentioning

confidence: 99%

Functional Characterization of a Novel BRCA1-Null Ovarian Cancer Cell Line in Response to Ionizing Radiation

DelloRusso

Welcsh

Wang

et al. 2007

Molecular Cancer Research

111

110

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The breast and ovarian cancer susceptibility gene BRCA1 plays a major role in the DNA damage response pathway. The lack of well-characterized human BRCA1-null cell lines has limited the investigation of BRCA1 function, particularly with regard to its role in ovarian cancer. We propagated a novel BRCA1-null human ovarian cancer cell line UWB1.289 from a tumor of papillary serous histology, the most common form of ovarian carcinoma. UWB1.289 carries a germline BRCA1 mutation within exon 11 and has a deletion of the wild-type allele. UWB1.289 is estrogen and progesterone receptor negative and has an acquired somatic mutation in p53, similar to the commonly used BRCA1-null breast cancer cell line HCC1937. We used ionizing radiation to induce DNA damage in both UWB1.289 and in a stable UWB1.289 line in which wild-type BRCA1 was restored. We examined several responses to DNA damage in these cell lines, including sensitivity to radiation, cell cycle checkpoint function, and changes in gene expression using microarray analysis. We observed that UWB1.289 is sensitive to ionizing radiation and lacks cell cycle checkpoint functions that are a normal part of the DNA damage response. Restoration of wild-type BRCA1 function in these cells partially restores DNA damage responses. Expression array analysis not only supports this partial functional correction but also reveals interesting new information regarding BRCA1-positive regulation of the expression of claudin 6 and other metastasis-associated genes and negative regulation of multiple IFN-inducible genes. (Mol Cancer Res 2007;5(1):35 -45)

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“…Additionally, some proteins (including IFI 16) also contain a newly identified Pyrin/PAAD/DAPIN protein-protein interaction domain toward their N-terminus (Choubey and Kotzin, 2002;Asefa et al, 2004). Based on the presence of protein-protein interaction domains, the p200 family proteins are thought to act as scaffolds to assemble protein complexes that regulate transcription of genes (Choubey and Kotzin, 2002;Xin et al, 2003).…”

Section: Discussionmentioning

confidence: 99%

“…The Ifi200 gene family encodes a family of IFNinducible proteins Johnstone and Trapani, 1999;Asefa et al, 2004). The family includes in mice Ifi202a, Ifi202b, Ifi203, Ifi204, and D3 genes; and in humans IFI16, MNDA, and AIM2 genes Wang et al, 1999).…”

Section: Introductionmentioning

confidence: 99%

Role of IFI 16 in cellular senescence of human fibroblasts

2004

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Defects in interferon (IFN) signaling that result in loss of expression of IFN-inducible proteins are associated with cellular immortalization, an important early event in the development of human cancer. Here we report that loss of IFN-inducible IFI 16 expression in human fibroblasts allows bypass of cellular senescence. We found that levels of IFI 16 mRNA and protein were higher in human old versus young fibroblasts and immortalization of fibroblasts with telomerase resulted in decreased expression of IFI 16. Moreover, overexpression of IFI 16 in immortalized fibroblasts strongly inhibited cell proliferation. Interestingly, knockdown of IFI 16 expression in fibroblasts inhibited p53-mediated transcription, downregulated p21 WAF1 expression, and extended the proliferation potential. Importantly, treatment of immortal cell lines with 5-aza-2 0 -deoxycytidine, an inhibitor of DNA methyltransferase, resulted in upregulation of IFI 16. Our observations support the idea that increased levels of IFI 16 in older populations of human fibroblasts contribute to cellular senescence.

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The interferon-inducible p200 family of proteins: a perspective on their roles in cell cycle regulation and differentiation

Cited by 123 publications

References 92 publications

New insights into MLL gene rearranged acute leukemias using gene expression profiling: shared pathways, lineage commitment, and partner genes

New insights into MLL gene rearranged acute leukemias using gene expression profiling: shared pathways, lineage commitment, and partner genes

Functional Characterization of a Novel BRCA1-Null Ovarian Cancer Cell Line in Response to Ionizing Radiation

Role of IFI 16 in cellular senescence of human fibroblasts

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