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The DOI matches its Crossref record; 6 of the 6 references it cites were found in a registry or an index.

Usp16 contributes to somatic stem-cell defects in Down’s syndrome

Adorno, Maddalena, Sikandar, Shaheen, Mitra, Siddhartha S., Kuo, Angera, Nicolis di Robilant, Benedetta, Haro-Acosta, Veronica, Ouadah, Youcef, Quarta, Marco, Rodriguez, Jacqueline, Qian, Dalong, Reddy, Vadiyala M., Cheshier, Samuel, Garner, Craig C., Clarke, Michael F.·2013·Nature
DOI 10.1038/nature12530PMC PMC3816928
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Crossref · 10.1038/nature12530

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  • USP16 is an antagonist of BMI1 and a de-repressor of Cdkn2a that acts through enzymatic removal of ubiquitin from histone H2A.

    “Upstream of Cdkn2a is USP16, an antagonist of BMI1 and a de-repressor of Cdkn2a that acts through the enzymatic removal of ubiquitin from histone H2A (Figure 4C; Adorno et al., 2013; Joo et al., 2007).”

    From Inhibiting USP16 rescues stem cell aging and memory in an Alzheimer’s model (2022) · cites this paper as Adorno et al., 2013

    The Results section reports that Usp16 opposes PRC1, can remove ubiquitin from histone H2A, and that reducing Usp16 lowers p16Ink4a and p19Arf expression at the Cdkn2a locus. It describes the proposed link between H2A deubiquitination and effects at that locus as strongly suggested, but says mutational analysis is needed to confirm the enzymatic mechanism. (LLM, conf=0.87)

    Experimental — accuracy not yet measured

  • USP16 counteracts self-renewal regulator BMI1 by deubiquitinating histone H2A on Lysine 119 at the Cdkn2a locus, resulting in increased expression of P16 (Ink4a) and P14 (Arf).

    “USP16 counteracts self-renewal regulator BMI1 by deubiquitinating histone H2A on Lysine 119 at the Cdkn2a locus, resulting in increased expression of protein products P16 (Ink4a) and P14 (Arf) (Adorno et al., 2013).”

    From Inhibiting USP16 rescues stem cell aging and memory in an Alzheimer’s model (2022) · cites this paper as Adorno et al., 2013

    In Results, under “Modulation of Ink4a/Arf by Usp16 in Ts65Dn cells” (page unavailable), the paper reports reduced H2AK119 ubiquitination at the Ink4a/Arf locus and increased p16Ink4a and p19Arf expression in mouse cells. It describes USP16-mediated removal of ubiquitin at this locus as a strongly suggested model requiring further testing, not a confirmed causal mechanism. The claim also names p14Arf, whereas the paper’s reported expression result concerns p19Arf. (LLM, conf=0.88)

    Experimental — accuracy not yet measured

  • Overexpression of USP16 in human-derived neurospheres leads to a marked decrease in formation of secondary neurospheres.

    “This is supported by previous data that showed overexpression of USP16 in human-derived neurospheres led to a marked decrease in the formation of secondary neurospheres (Adorno et al., 2013), and overexpression of Bmi1 led to increased self-renewal and maintenance of multipotency (Fasano et al., 2009).”

    From Inhibiting USP16 rescues stem cell aging and memory in an Alzheimer’s model (2022) · cites this paper as Adorno et al., 2013

  • Increased expression of P16 and P14 results in increased senescence with a concomitant decrease in self-renewal.

    “This results in increased senescence with a concomitant decrease in self-renewal.”

    From Inhibiting USP16 rescues stem cell aging and memory in an Alzheimer’s model (2022) · cites this paper as Adorno et al., 2013

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Citations

Cites

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Research works printed but not linked: 33

  1. Antonarakis, S. E., Lyle, R., Dermitzakis, E. T., Reymond, A. & Deutsch, S. Chromosome 21 and Down syndrome: from genomics to pathophysiology. Nature Rev. Genet. 5, 725–738 (2004) · DOI · Paper page
  2. Yang, Q., Rasmussen, S. A. & Friedman, J. M. Mortality associated with Down’s syndrome in the USA from 1983 to 1997: a population-based study. Lancet 359, 1019–1025 (2002) · DOI
  3. Roth, G. M., Sun, B., Greensite, F. S., Lott, I. T. & Dietrich, R. B. Premature aging in persons with Down syndrome: MR findings. Am. J. Neuroradiol. 17, 1283–1289 (1996)
  4. Zigman, W. B. & Lott, I. T. Alzheimer’s disease in Down syndrome: neurobiology and risk. Ment. Retard. Dev. Disabil. Res. Rev. 13, 237–246 (2007) · DOI
  5. Liu, L. & Rando, T. A. Manifestations and mechanisms of stem cell aging. J. Cell Biol. 193, 257–266 (2011) · DOI
  6. Sago, H. et al. Genetic dissection of region associated with behavioral abnormalities in mouse models for Down syndrome. Pediatr. Res. 48, 606–613 (2000) · DOI
  7. Joo, H.-Y. et al. Regulation of cell cycle progression and gene expression by H2A deubiquitination. Nature 449, 1068–1072 (2007) · DOI · Paper page
  8. Lorenzo, L. P. E. et al. Defective hematopoietic stem cell and lymphoid progenitor development in the Ts65Dn mouse model of Down syndrome: potential role of oxidative stress. Antioxid. Redox Signal. 15, 2083–2094 (2011) · DOI
  9. Chao, M. P., Seita, J. & Weissman, I. L. Establishment of a normal hematopoietic and leukemia stem cell hierarchy. Cold Spring Harb. Symp. Quant. Biol. 73, 439–449 (2008) · DOI
  10. Akala, O. O. et al. Long-term haematopoietic reconstitution by Trp53−/−p16Ink4a−/−p19Arf−/− multipotent progenitors. Nature 453, 228–232 (2008) · DOI
  11. Pietersen, A. M. et al. Bmi1 regulates stem cells and proliferation and differentiation of committed cells in mammary epithelium. Curr. Biol. 18, 1094–1099 (2008) · DOI
  12. Molofsky, A. V. et al. Bmi-1 dependence distinguishes neural stem cell self-renewal from progenitor proliferation. Nature 425, 962–967 (2003) · DOI
  13. Cao, G. et al. Bmi-1 absence causes premature brain degeneration. PLoS ONE 7, e32015 (2012) · DOI
  14. Lorenzi, H. A. & Reeves, R. H. Hippocampal hypocellularity in the Ts65Dn mouse originates early in development. Brain Res. 1104, 153–159 (2006) · DOI · Paper page
  15. Ellis, P. et al. SOX2, a persistent marker for multipotential neural stem cells derived from embryonic stem cells, the embryo or the adult. Dev. Neurosci. 26, 148–165 (2004) · DOI
  16. Fischer, J. et al. Prospective isolation of adult neural stem cells from the mouse subependymal zone. Nature Protocols 6, 1981–1989 (2011) · DOI · Paper page
  17. Pastrana, E., Cheng, L.-C. & Doetsch, F. Simultaneous prospective purification of adult subventricular zone neural stem cells and their progeny. Proc. Natl Acad. Sci. USA 106, 6387–6392 (2009) · DOI
  18. Stingl, J. et al. Purification and unique properties of mammary epithelial stem cells. Nature 439, 993–997 (2006) · DOI
  19. Jacobs, J. J., Kieboom, K., Marino, S., DePinho, R. A. & van Lohuizen, M. The oncogene and Polycomb-group gene bmi-1 regulates cell proliferation and senescence through the ink4a locus. Nature 397, 164–168 (1999) · DOI · Paper page
  20. Liu, Y. et al. Expression of p16 INK4a in peripheral blood T-cells is a biomarker of human aging. Aging Cell 8, 439–448 (2009) · DOI · Paper page
  21. Kimura, M. et al. Proliferation dynamics in cultured skin fibroblasts from Down syndrome subjects. Free Radic. Biol. Med. 39, 374–380 (2005) · DOI
  22. Carmeliet, G., David, G. & Cassiman, J. J. Cellular ageing of Alzheimer’s disease and Down syndrome cells in culture. Mutat. Res. 256, 221–231 (1991) · DOI
  23. Arron, J. R. et al. NFAT dysregulation by increased dosage of DSCR1 and DYRK1A on chromosome 21. Nature 441, 595–600 (2006) · DOI · Paper page
  24. Roy, A. et al. Perturbation of fetal liver hematopoietic stem and progenitor cell development by trisomy 21. Proc. Natl Acad. Sci. USA 109, 17579–17584 (2012) · DOI
  25. Reinholdt, L. G. et al. Molecular characterization of the translocation breakpoints in the Down syndrome mouse model Ts65Dn. Mamm. Genome 22, 685–691 (2011) · DOI · Paper page
  26. Hu, Y. & Smyth, G. K. ELDA: extreme limiting dilution analysis for comparing depleted and enriched populations in stem cell and other assays. J. Immunol. Methods 347, 70–78 (2009) · DOI
  27. Dalerba, P. et al. Single-cell dissection of transcriptional heterogeneity in human colon tumors. Nature Biotechnol. 29, 1120–1127 (2011) · DOI
  28. Zeng, Y. A. & Nusse, R. Wnt proteins are self-renewal factors for mammary stem cells and promote their long-term expansion in culture. Cell Stem Cell 6, 568–577 (2010) · DOI
  29. Negishi, M. et al. A novel zinc finger protein Zfp277 mediates transcriptional repression of the Ink4a/arf locus through polycomb repressive complex 1. PLoS ONE 5, e12373 (2010) · DOI
  30. Ventura, A. et al. Cre-lox-regulated conditional RNA interference from transgenes. Proc. Natl Acad. Sci. USA 101, 10380–10385 (2004) · DOI
  31. Shimono, Y. et al. Downregulation of miRNA-200c links breast cancer stem cells with normal stem cells. Cell 138, 592–603 (2009) · DOI
  32. Tiscornia, G., Singer, O. & Verma, I. M. Production and purification of lentiviral vectors. Nature Protocols 1, 241–245 (2006) · DOI
  33. Majeti, R., Park, C. Y. & Weissman, I. L. Identification of a hierarchy of multipotent hematopoietic progenitors in human cord blood. Cell Stem Cell. 1, 635–645 (2007) · DOI

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Metadata

Authors
Adorno, M., Sikandar, S., Mitra, S. S., Kuo, A., Nicolis di Robilant, B., Haro-Acosta, V., Ouadah, Y., Quarta, M., Rodriguez, J., Qian, D., Reddy, V. M., Cheshier, S., Garner, C. C., & Clarke, M. F.
Venue
Nature
Publisher
Springer Science and Business Media LLC
Published
2013-09-11
Volume
501
Issue
7467
Pages
380-384
ISSN
  • 0028-0836
  • 1476-4687
DOI
10.1038/nature12530
PMC
PMC3816928
Cited by
134
References
6
Language
en
Licence

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