scispace - formally typeset
Y

Yuko Futahashi

Researcher at National Institutes of Health

Publications -  12
Citations -  240

Yuko Futahashi is an academic researcher from National Institutes of Health. The author has contributed to research in topics: P-TEFb & Cyclin A. The author has an hindex of 9, co-authored 12 publications receiving 235 citations.

Papers
More filters
Journal ArticleDOI

Ligand-independent higher-order multimerization of CXCR4, a G-protein-coupled chemokine receptor involved in targeted metastasis

TL;DR: It is hypothesized that CXCR4 distributes to the cell surface as a multimer, in order to effectively sense, with increased avidity, the chemotaxis‐inducing ligand in the microenvironment, and this is the first report providing direct experimental evidence for the higher‐order multimerization of CX CR4 in vivo.
Journal ArticleDOI

Separate elements are required for ligand-dependent and -independent internalization of metastatic potentiator CXCR4

TL;DR: Analysis of the role of the CXCR4 cytoplasmic tail in steady‐state internalization using the NP2 cell line demonstrates that ligand‐dependent and ‐independent internalization is genetically separable and that, between amino acids 336 and 342, there is a negative regulatory element for ligand-promoted internalization.
Journal ArticleDOI

Substitution of the myristoylation signal of human immunodeficiency virus type 1 Pr55Gag with the phospholipase C-δ1 pleckstrin homology domain results in infectious pseudovirion production

TL;DR: This study replaced the myristoylation signal of MA with a well-studied phosphatidylinositol 4,5-biphosphate-binding plasma membrane (PM) targeting motif, the phospholipase C-δ1 pleckstrin homology (PH) domain, and demonstrated infectious pseudovirion production without myristoyslated Pr55Gag.
Journal ArticleDOI

Inhibiting lentiviral replication by HEXIM1, a cellular negative regulator of the CDK9/cyclin T complex.

TL;DR: Data indicate that HEXIM1 is a host factor that negatively regulates lentiviral replication specifically, and elucidating the regulatory mechanism of HexIM1 might lead to ways to control lentivirus replication.