Cracking the ANP32 whips: Important functions, unequal requirement, and hints at disease implications

Reilly, Patrick T.; Yu, Yun; Hamiche, Ali; Wang, Lishun

doi:10.1002/bies.201400058

Cited by 86 publications

(95 citation statements)

References 118 publications

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“…The multifunctional ANP32A protein was originally identified as an inhibitor of protein phosphatase 2 A (Li et al, 1996) and has been assigned a variety of physiological functions, including repression of transcription and export of specific mRNAs from the nucleus (see Reilly et al, 2014). In particular, ANP32A has been reported to interact with STAT1 and STAT2 in HeLa cells exposed to IFNβ, and to be required for binding of STAT-containing transcriptional activators to the promoters of ISGs (Kadota and Nagata, 2011).…”

Section: Resultsmentioning

confidence: 99%

Normal human cell proteins that interact with the adenovirus type 5 E1B 55 kDa protein

Hung

Flint

2017

Virology

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Several of the functions of the human adenovirus type 5 E1B 55 kDa protein are fulfilled via the virus-specific E3 ubiquitin ligase it forms with the viral E4 Orf6 protein and several cellular proteins. Important substrates of this enzyme have not been identified, and other functions, including repression of transcription of interferon-sensitive genes, do not require the ligase. We therefore used immunoaffinity purification and liquid chromatography-mass spectrometry of lysates of normal human cells infected in parallel with HAdV-C5 and E1B 55 kDa protein-null mutant viruses to identify specifically E1B 55 kDa-associated proteins. The resulting set of > 90 E1B-associated proteins contained the great majority identified previously, and was enriched for those associated with the ubiquitin-proteasome system, RNA metabolism and the cell cycle. We also report very severe inhibition of viral genome replication when cells were exposed to both specific or non-specific siRNAs and interferon prior to infection.

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Section: Resultsmentioning

confidence: 99%

Normal human cell proteins that interact with the adenovirus type 5 E1B 55 kDa protein

Hung

Flint

2017

Virology

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“…H2A.Z is rapidly removed from the DSB through the combined action of ANP32E, an H2A.Z-specific histone chaperone 41; 97; 98 and the Ino80 remodeling complex 85 . ANP32E is a member of the acidic, leucine rich phosphoprotein ANP32 family implicated in apoptosis, phosphatase inhibition, intracellular transport and many cancers 99 . ANP32E binds to a unique sequence in the c-terminal docking domain of H2A.Z, catalyzing the removal of the entire H2A.Z-H2B dimer 97; 98 .…”

Section: Transitioning From Repressive To Open Chromatinmentioning

confidence: 99%

Patching Broken DNA: Nucleosome Dynamics and the Repair of DNA Breaks

Gürsoy-Yüzügüllü

House

Price

2016

Journal of Molecular Biology

116

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The ability of cells to detect and repair DNA double-strand breaks (DSBs) is dependent on reorganization of the surrounding chromatin structure by chromatin remodeling complexes. These complexes promote access to the site of DNA damage, facilitate processing of the damaged DNA and, importantly, are essential to repackage the repaired DNA. Here, we will review the chromatin remodeling steps which occur immediately after DSB production and which prepare the damaged chromatin template for processing by the DSB repair machinery. DSBs promote rapid accumulation of repressive complexes, including HP1, the NuRD complex, H2A.Z and histone methyltransferases at the DSB. This shift to a repressive chromatin organization may be important to inhibit local transcription and limit mobility of the break, and to maintain the DNA ends in close contact. Subsequently, the repressive chromatin is rapidly dismantled through a mechanism involving dynamic exchange of the histone variant H2A.Z. H2A.Z removal at DSBs alters the acidic patch on the nucleosome surface, promoting acetylation of the H4 tail (by the NuA4-Tip60 complex) and shifting the chromatin to a more open structure. Further, H2A.Z removal promotes chromatin ubiquitination and recruitment of additional DSB repair proteins to the break. Modulation of the nucleosome surface and nucleosome function during DSB repair therefore plays a vital role in processing of DNA breaks. Further, the nucleosome surface may function as a central hub during DSB repair, directing specific patterns of histone modification, recruiting DNA repair proteins and modulating chromatin packing during processing of the damaged DNA template.

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“…Anp32a was chosen as hub gene which was down regulated (p-value= 2.29E-06) in the plum1 module by comparing control group. ANP32 proteins are implicated in cell differentiation, apoptotic cell death and cell proliferation (Reilly et al, 2014). ANP32A were recognized as tumor suppressor by inhibiting cell transformation (Reilly et al, 2014).…”

Section: Discussionmentioning

confidence: 99%

“…ANP32 proteins are implicated in cell differentiation, apoptotic cell death and cell proliferation (Reilly et al, 2014). ANP32A were recognized as tumor suppressor by inhibiting cell transformation (Reilly et al, 2014). Its expression level was deregulated in the breast, prostate cancer but up regulated in colorectal and liver cancer.…”

Section: Discussionmentioning

confidence: 99%

Identification of Specific Gene Modules in Mouse Lung Tissue Exposed to Cigarette Smoke

Xing

Zhang²,

Lu³

et al. 2015

Asian Pacific Journal of Cancer Prevention

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Background: Exposure to cigarette may affect human health and increase risk of a wide range of diseases including pulmonary diseases, such as chronic obstructive pulmonary disease (COPD), asthma, lung fibrosis and lung cancer. However, the molecular mechanisms of pathogenesis induced by cigarettes still remain obscure even with extensive studies. With systemic view, we attempted to identify the specific gene modules that might relate to injury caused by cigarette smoke and identify hub genes for potential therapeutic targets or biomarkers from specific gene modules. Materials and Methods: The dataset GSE18344 was downloaded from the Gene Expression Omnibus (GEO) and divided into mouse cigarette smoke exposure and control groups. Subsequently, weighted gene co-expression network analysis (WGCNA) was used to construct a gene co-expression network for each group and detected specific gene modules of cigarette smoke exposure by comparison. Results: A total of ten specific gene modules were identified only in the cigarette smoke exposure group but not in the control group. Seven hub genes were identified as well, including Fip1l1, Anp32a, Acsl4, Evl, Sdc1, Arap3 and Cd52. Conclusions: Specific gene modules may provide better understanding of molecular mechanisms, and hub genes are potential candidates of therapeutic targets that may possible improve development of novel treatment approaches.

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Cracking the ANP32 whips: Important functions, unequal requirement, and hints at disease implications

Cited by 86 publications

References 118 publications

Normal human cell proteins that interact with the adenovirus type 5 E1B 55 kDa protein

Normal human cell proteins that interact with the adenovirus type 5 E1B 55 kDa protein

Patching Broken DNA: Nucleosome Dynamics and the Repair of DNA Breaks

Identification of Specific Gene Modules in Mouse Lung Tissue Exposed to Cigarette Smoke

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