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Jeong Hee Hong

Researcher at Gachon University

Publications -  68
Citations -  2088

Jeong Hee Hong is an academic researcher from Gachon University. The author has contributed to research in topics: Medicine & Intracellular. The author has an hindex of 22, co-authored 55 publications receiving 1770 citations. Previous affiliations of Jeong Hee Hong include Yonsei University & National Institutes of Health.

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Carbon nanotubes as cancer therapeutic carriers and mediators

TL;DR: If limitations such as a long-term cytotoxicity in the body, lack of size uniformity during the synthetic process, loading deviations for drug–CNT complexes, and release controllability at the target point are overcome, CNTs will become one of the strongest tools that are available for various other biomedical fields as well as for cancer therapy.

Mite and cockroach allergens activate protease-activated receptor 2 and delay epidermal permeability barrier recovery

TL;DR: In this article, the effects of both allergens on the epidermal barrier function as well as on the Epidermal calcium gradient were investigated, and it was shown that when applied on the barrier-disrupted site, increased protease activities in the epIDERmis and delayed barrier recovery and lamellar body secretion in murine skin.
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Mite and cockroach allergens activate protease-activated receptor 2 and delay epidermal permeability barrier recovery

TL;DR: It is suggested that allergens with protease activity can influence the epidermal permeability barrier homeostasis through PAR-2 activation and consequent modulation of the calcium ions in skin.
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An endoplasmic reticulum/plasma membrane junction: STIM1/Orai1/TRPCs

TL;DR: Recent findings on how STIM1 gates and regulates the Orais and TRPCs, and how theSTIM1/Orai1/TRPCs complexes may function in vivo to mediate SOC activity are discussed.
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Deletion of TRPC3 in Mice Reduces Store-Operated Ca2+ Influx and the Severity of Acute Pancreatitis

TL;DR: These findings establish the native TRPC3 as an SOC in vivo and a role for TR PC3-mediated Ca(2+) influx in the pathogenesis of acute pancreatitis and suggest thatTRPC3 should be considered a target for prevention of pancreatic damage in acute pancreatita.