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| 1 | “Tailored”organometallics as precursors for the chemicalvapor deposition of high-purity palladium and platinum thinfilms显示文摘 | John E Gozum Deborah M Pollina James A Jensen | 1988 | J Am Chem Soc1988，110，： | 1 |
| 2 | Regulating the angiogenic balance in tissues显示文摘 | Pollina EA Legesse-Miller A Haley EM | 2008 | Cell Cycle2008，7，13： | 1 |
| 3 | Placental monocyte infiltrates in response to Plasmodiumfalciparum malaria infection and their association with adverse pregnancy outcomes 显示文摘 | Rogerson SJ Pollina E Getachew A | 2003 | Am J Trop Med Hyg2003，68，1： | 1 |
| 4 | Coagulation factors and recur- rence of ischemic and bleeding adverse events in patients with acute coronary syndromes显示文摘 | Campo G Pavasini R Pollina A | 2013 | Thromb Res2013，132，2： | 1 |
| 5 | The tomato carotenoid cleavage dioxygenase8 (SlCCD8) regulates rhizosphere signaling,plant architecture and affects reproductive development through strigolactone biosynthesis显示文摘 | Kohlen W Charnikhova T Lammers M Pollina T Toth P Haider I Pozo M J de Maagd R A Ruyter-Spira C Bouwmeester H J | 2012 | The New Phytologist2012，196，2： | 1 |
| 6 | Eetopie expression of hone sialoprotein in human thyroid cancer显示文摘 | BELLAHCENE A ALBERT V POLLINA L | 1998 | Thyroid1998，8，8： | 1 |
| 7 | On-treatment platelet reactivity in patients with chronic obstructive pulmonary disease undergoing percutaneous coronary intervention 显示文摘 | Campo G Pavasini R Pollina A | 2014 | Thorax2014，69，1： | 1 |
| 8 | Ectopic expres- sion of bone sialoprotein in human thyroid cancer 显示文摘 | Bellahcene A Albert V Pollina L | 1998 | Thyroid1998，8，8： | 1 |
| 9 | Epigenetic regulation of aging stem cells 显示文摘 | Pollina EA Brunet A | 2011 | Oncogene2011，30，28： | 1 |
| 10 | 'Tailored' organometallics as precursors for the chemical vapor deposition of high-purity palladium and platinum thin films显示文摘 | Gozum J E Pollina D M Jensen J A | 1988 | J Am Chem Soc1988，110，33： | 1 |
| 11 | A NPAS4-NuA4 complex couples synaptic activity to DNA repair显示文摘Neuronal activity is crucial for adaptive circuit remodelling but poses an inherent risk to the stability of the genome acrossthe long lifespan of postmitotic neurons1-5. Whether neurons have acquired specialized genome protection mechanisms thatenable them to withstand decades of potentially damaging stimuli during periods of heightened activity is unknown. Here weidentify an activity-dependent DNA repair mechanism in which a new form of the NuA4-TIP60 chromatin modifier assembles inactivated neurons around the inducible, neuronal-specific transcription factor NPAS4. We purify this complex from the brain anddemonstrate its functions in eliciting activity-dependent changes to neuronal transcriptomes and circuitry. By characterizing thelandscape of activity-induced DNA double-strand breaks in the brain, we show that NPAS4-NuA4 binds to recurrently damagedregulatory elements and recruits additional DNA repair machinery to stimulate their repair. Gene regulatory elements bound byNPAS4-NuA4 are partially protected against age-dependent accumulation of somatic mutations. Impaired NPAS4-NuA4signalling leads to a cascade of cellular defects, including dysregulated activity-dependent transcriptional responses, loss of controlover neuronal inhibition and genome instability, which all culminate to reduce organismal lifespan. In addition, mutations inseveral components of the NuA4 complex are reported to lead to neurodevelopmental and autism spectrum disorders. Together,these findings identify a neuronal-specific complex that couples neuronal activity directly to genome preservation, the disruptionof which may contribute to developmental disorders, neurodegeneration and ageing. | Elizabeth A Pollina | 2023 | 四川生理科学杂志2023，45，2： | 0 |
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