909 resultados para Howe, Richard Howe, Earl, 1726-1799
Resumo:
Mode of access: Internet.
Resumo:
NUC pre-1956
Resumo:
Signatures: [A]⁴(-[A]1) B-P⁴ Q⁴(-Q4).
Resumo:
Mode of access: Internet.
Resumo:
continued: ... XII. Historical documents and remarks (from December, 1799 to March, 1801) ; Trial of Cooper ; Emigration Society ; Washington's death ; Proceedings in Congress during the session which began December, 1799 ; Board of Commissioners ; Defence of the Quakers of Pennsylvania ; Farewell advertisement ; Prison eclogue ; Republican morality ; Jefferson's election ; Adam's public conduct ; Jefferson's character ; Convention concluded between America and France, in 1800 ; Proceedings in Congress during the session which ended in March, 1801 ; Index.
Resumo:
Mode of access: Internet.
Resumo:
Mode of access: Internet.
Resumo:
Mode of access: Internet.
Resumo:
Mode of access: Internet.
Resumo:
STC (2nd ed.) gives W. Howe as actual printer.
Resumo:
References: Blanck. Bibl. Amer. lit. 129.
Resumo:
Ataxia-oculomotor apraxia (AOA1) is a neurological disorder with symptoms that overlap those of ataxia-telangiectasia, a syndrome characterized by abnormal responses to double-strand DNA breaks and genome instability. The gene mutated in AOA1, APTX, is predicted to code for a protein called aprataxin that contains domains of homology with proteins involved in DNA damage signalling and repair. We demonstrate that aprataxin is a nuclear protein, present in both the nucleoplasm and the nucleolus. Mutations in the APTX gene destabilize the aprataxin protein, and fusion constructs of enhanced green fluorescent protein and aprataxin, representing deletions of putative functional domains, generate highly unstable products. Cells from AOA1 patients are characterized by enhanced sensitivity to agents that cause single-strand breaks in DNA but there is no evidence for a gross defect in single-strand break repair. Sensitivity to hydrogen peroxide and the resulting genome instability are corrected by transfection with full-length aprataxin cDNA. We also demonstrate that aprataxin interacts with the repair proteins XRCC1, PARP-1 and p53 and that it co-localizes with XRCC1 along charged particle tracks on chromatin. These results demonstrate that aprataxin influences the cellular response to genotoxic stress very likely by its capacity to interact with a number of proteins involved in DNA repair.
Resumo:
The Structural Genomics Consortium (SGC) and its clinical, industry and disease-foundation partners are launching open-source preclinical translational medicine studies.