scispace - formally typeset
G

Giovanna Tabellini

Researcher at University of Brescia

Publications -  87
Citations -  4906

Giovanna Tabellini is an academic researcher from University of Brescia. The author has contributed to research in topics: PI3K/AKT/mTOR pathway & Protein kinase B. The author has an hindex of 37, co-authored 83 publications receiving 4400 citations. Previous affiliations of Giovanna Tabellini include University of Trieste & Brescia University.

Papers
More filters
Journal ArticleDOI

The role of chemerin in the colocalization of NK and dendritic cell subsets into inflamed tissues.

TL;DR: A role for the ChemR23/chemerin axis in the recruitment of blood NK cells is proposed and chemerin is strongly implicate as a key factor for the colocalization of NK cells and DC subsets in pathologic peripheral tissues.
Journal ArticleDOI

Identification of a subset of human natural killer cells expressing high levels of programmed death 1: A phenotypic and functional characterization.

TL;DR: A novel subpopulation of human NK cells expressing high levels of PD‐1 is identified and characterized, which have the phenotypic characteristics of fully mature NK cells and are increased in patients with ovarian carcinoma.
Journal ArticleDOI

Phosphoinositide 3-kinase/Akt signaling pathway and its therapeutical implications for human acute myeloid leukemia.

TL;DR: The existing knowledge about PI3K/Akt signaling in AML cells is summarized, the rationale for targeting this fundamental signal transduction network by means of selective pharmacological inhibitors is examined and this pathway is an attractive target for the development of novel anticancer strategies.
Journal ArticleDOI

The emerging multiple roles of nuclear Akt

TL;DR: Evidence accumulated over the past 15 years has highlighted the presence of active Akt in the nucleus, where it acts as a fundamental component of key signaling pathways, and the most relevant findings about nuclear Akt are summarized.
Journal ArticleDOI

A new selective AKT pharmacological inhibitor reduces resistance to chemotherapeutic drugs, TRAIL, all-trans-retinoic acid, and ionizing radiation of human leukemia cells.

TL;DR: Testing whether or not a new selective Akt inhibitor was as effective as Ly294002 in lowering the sensitivity threshold of HL60 cells to chemotherapeutic drugs, TRAIL, ATRA, and ionizing radiation indicates that selective AkT pharmacological inhibitors might be used in the future for enhancing the sensitivity of leukemia cells to therapeutic treatments that induce apoptosis or for overcoming resistance to these treatments.