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Giuseppe Biamonti

Researcher at National Research Council

Publications -  16
Citations -  321

Giuseppe Biamonti is an academic researcher from National Research Council. The author has contributed to research in topics: DNA ligase & Ribonucleoprotein. The author has an hindex of 8, co-authored 16 publications receiving 293 citations. Previous affiliations of Giuseppe Biamonti include Istituto Superiore di Sanità.

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cDNA cloning of human hnRNP protein A1 reveals the existence of multiple mRNA isoforms

TL;DR: Analysis of genomic DNA showed at least 30 A1-specific sequences, some of which correspond to processed pseudogenes and suggest that protein A1 is encoded by a multigene family.
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The N-terminal domain of human DNA ligase I contains the nuclear localization signal and directs the enzyme to sites of DNA replication

TL;DR: It is shown thatDNA ligase I, the main DNA ligase activity in proliferating cells, associates with the factories during S phase but displays a diffuse nucleoplasmic distribution in non‐S phase nuclei, and proposed that in vivo the activity of DNA ligases I could be modulated through the control of its sub‐nuclear compartmentalization.
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Phosphorylation of SRSF1 is modulated by replicational stress

TL;DR: Observations indicate that a relevant aspect of the cell response to DNA damage involves the post-translational regulation of splicing factor SRSF1 which is associated with a shift in the alternative splicing program of target genes to control cell survival or cell death.
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Identification of autoantibodies to the I protein of the heterogeneous nuclear ribonucleoprotein complex in patients with systemic sclerosis

TL;DR: Human autoimmune sera show distinct patterns of anti-hnRNP reactivity, i.e., anti-A/B in SLE and RA sera, and anti-I in SSc sera; this suggests that A/B proteins and the I protein may be involved in different dynamic hnRNP complexes that elicit different autoimmune responses.
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An Intricate Connection between Alternative Splicing and Phenotypic Plasticity in Development and Cancer.

TL;DR: Unravelling the intricate relationship between AS and the maintenance of a stem-like phenotype may explain molecular mechanisms underlying cancer cell plasticity and improve cancer diagnosis and treatment.