scispace - formally typeset
A

Aya Nagaoka

Researcher at Kao Corporation

Publications -  8
Citations -  399

Aya Nagaoka is an academic researcher from Kao Corporation. The author has contributed to research in topics: Hyaluronic acid & Synovial membrane. The author has an hindex of 6, co-authored 8 publications receiving 287 citations.

Papers
More filters
Journal ArticleDOI

KIAA1199, a deafness gene of unknown function, is a new hyaluronan binding protein involved in hyaluronan depolymerization

TL;DR: KIAA1199 is a unique hyaladherin with a key role in HA catabolism in the dermis of the skin and arthritic synovium, and transfection of KIAA 1199 cDNA into cells conferred the ability to catabolize HA in an endo-β-N-acetylglucosaminidase–dependent manner via the clathrin-coated pit pathway.
Journal ArticleDOI

Regulation of Hyaluronan (HA) Metabolism Mediated by HYBID (Hyaluronan-binding Protein Involved in HA Depolymerization, KIAA1199) and HA Synthases in Growth Factor-stimulated Fibroblasts *

TL;DR: It is suggested that inefficient down-regulation of HYBID by TGF-β1 in arthritic synovial fibroblasts may be linked to accumulation of depolymerized HA insynovial fluids in arthritis patients.
Journal ArticleDOI

Murine homologue of the human KIAA1199 is implicated in hyaluronan binding and depolymerization

TL;DR: It is shown that cells transfected with mKiaa1199 cDNA selectively catabolized HA via the clathrin‐coated pit pathway, and it is concluded that like hKIAA1199, mKIAa 1199 is a hyaladherin leading to HA depolymerization.
Journal ArticleDOI

N-terminal signal sequence is required for cellular trafficking and hyaluronan-depolymerization of KIAA1199

TL;DR: It is shown that the cleavage of N‐terminal 30 amino acids occurs in functionally matured KIAA1199, and the deletion of the N-terminal portion results in altered intracellular trafficking of the molecule and loss of cellular HA depolymerization.
Journal ArticleDOI

Reduction of hyaluronan and increased expression of HYBID (alias CEMIP and KIAA1199) correlate with clinical symptoms in photoaged skin.

TL;DR: It is shown that photoageing‐dependent changes in HA and their molecular mechanisms, and the relationship between HA metabolism and clinical symptoms in photoaged skin remain elusive.