Nuclear receptor binding protein 1 regulates intestinal progenitor cell homeostasis and tumour formation

Wilson, Catherine H.; Crombie, Catriona; Weyden, Louise van der; Poulogiannis, George; Rust, Alistair G.; Pardo, Mercedes; Gracia, Tannia; Yu, Lu; Choudhary, Jyoti S.; Poulin, Gino; McIntyre, Rebecca E; Winton, Douglas J.; March, H. Nikki; Arends, Mark J.; Fraser, Andrew G.; Adams, David J.

doi:10.1038/emboj.2012.91

Cited by 43 publications

(57 citation statements)

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“…We identified NRBP1 as an interacting protein of TSC22D2 in our yeast two-hybrid screen. NRBP1 is a conserved regulator of cell fate and plays an important role in tumor suppression [45][46][47]. In Caenorhabditis elegans, the somatic loss of Nrbp1 was shown to result in tumorigenesis and the accumulation of Tsc22d2 [45].…”

Section: Discussionmentioning

confidence: 99%

Yeast two-hybrid screening identified WDR77 as a novel interacting partner of TSC22D2

et al. 2016

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Transforming growth factor β-stimulated clone 22 domain family, member 2 (TSC22D2), a member of the TSC22D family, has been implicated as a tumor-associated gene, but its function remains unknown. To further explore its biological role, yeast two-hybrid screening combined with multiple bioinformatics tools was used to identify 44 potential interacting partners of the TSC22D2 protein that were mainly involved in gene transcription, cellular metabolism, and cell cycle regulation. The protein WD repeat domain 77 (WDR77) was selected for further validation due to its function in the cell cycle and tumor development, as well as its high detection frequency in the yeast two-hybrid assay. Immunoprecipitation and immunofluorescence experiments confirmed an interaction between the TSC22D2 and WDR77 proteins. Our work greatly expands the putative protein interaction network of TSC22D2 and provides deeper insight into the biological functions of the TSC22D2 and WDR77 proteins.

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Section: Discussionmentioning

confidence: 99%

Yeast two-hybrid screening identified WDR77 as a novel interacting partner of TSC22D2

et al. 2016

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“…Post-translational modifications of SALL4 such as phosphorylation 13 , ubiquitination 14 and sumoylation 15 have been reported. The functions of these post-translational modifications are largely unknown.…”

Section: Introductionmentioning

confidence: 99%

SALL4, the missing link between stem cells, development and cancer

Tatetsu

Kong

Gao

et al. 2016

Gene

109

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There is a growing body of evidence supporting that cancer cells share many similarities with embryonic stem cells (ESCs). For example, aggressive cancers and ESCs share a common gene expression signature that includes hundreds of genes. Since ESC genes are not present in most adult tissues, they could be ideal candidate targets for cancer-specific diagnosis and treatment. This is an exciting cancer-targeting model. The major hurdle to test this model is to identify the key factors/pathway(s) within ESCs that are responsible for the cancer phenotype. SALL4 is one of few genes that can establish this link. The first publication of SALL4 is on its mutation in a human inherited disorder with multiple developmental defects. Since then, over 300 papers have been published on various aspects of this gene in stem cells, development, and cancers. This review aims to summarize our current knowledge of SALL4, including a SALL4-based approach to classify and target cancers. Many questions about this important gene still remain unanswered, specifically, on how this gene regulates cell fates at a molecular level. Understanding SALL4’s molecular functions will allow development of specific targeted approaches in the future.

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“…Gene NRBP1 is a conserved regulator of cell fate and plays an important role in tumor suppression. A low NRBP1 expression level is associated with a poorer prognosis of LUAD (Wilson et al., ). Gene RAP1B is a key suppressor of neutrophil migration and lung inflammation, and a reduced RAP1B prenylation has been detected in lung cancer cell lines.…”

Section: Discussionmentioning

confidence: 99%

Accommodating missingness in environmental measurements in gene‐environment interaction analysis

Zang

Zhang

et al. 2017

Genetic Epidemiology

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For the prognosis of complex diseases, beyond the main effects of genetic (G) and environmental (E) factors, gene-environment (G-E) interactions also play an important role. Many approaches have been developed for detecting important G-E interactions, most of which assume that measurements are complete. In practical data analysis, missingness in E measurements are not uncommon, and failing to properly accommodate such missingness leads to biased estimation and false marker identification. In this study, we conduct G-E interaction analysis with prognosis data under an accelerated failure time (AFT) model. To accommodate missingness in E measurements, we adopt a nonparametric kernel-based data augmentation approach. With a well-designed weighting scheme, a nice “byproduct” is that the proposed approach enjoys a certain robustness property. A penalization approach, which respects the “main effects, interactions” hierarchy, is adopted for selection (of important interactions and main effects) and regularized estimation. The proposed approach has sound interpretations and a solid statistical basis. It outperforms multiple alternatives in simulation. The analysis of TCGA data on lung cancer and melanoma leads to interesting findings and models with superior prediction.

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Nuclear receptor binding protein 1 regulates intestinal progenitor cell homeostasis and tumour formation

Cited by 43 publications

References 50 publications

Yeast two-hybrid screening identified WDR77 as a novel interacting partner of TSC22D2

Yeast two-hybrid screening identified WDR77 as a novel interacting partner of TSC22D2

SALL4, the missing link between stem cells, development and cancer

Accommodating missingness in environmental measurements in gene‐environment interaction analysis

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