Connexin hemichannels influence genetically determined inflammatory and hyperproliferative skin diseases

Noah A. Levit; Thomas W. White

doi:10.1016/j.phrs.2015.07.015

Connexin hemichannels influence genetically determined inflammatory and hyperproliferative skin diseases

Noah A. Levit
, Thomas W. White

Physiology and Biophysics

Stony Brook University

Research output: Contribution to journal › Article › peer-review

16 Scopus citations

Abstract

Connexin mutations underlie numerous human genetic diseases. Several connexin genes have been linked to skin diseases, and mechanistic studies have indicated that a gain of abnormal channel function may be responsible for pathology. The topical accessibility of the epidermal connexins, the existence of several mouse models of human skin disease, and the ongoing identification of pharmacological inhibitors targeting connexins provide an opportunity to test new therapeutic approaches.

Original language	English
Pages (from-to)	337-343
Number of pages	7
Journal	Pharmacological Research
Volume	99
DOIs	https://doi.org/10.1016/j.phrs.2015.07.015
State	Published - Jul 30 2015

Keywords

Connexin
Gap junctions
Genetic disease
Inflammation
Inhibitor
KID syndrome
Skin

Access to Document

10.1016/j.phrs.2015.07.015

Cite this

@article{0cbe9274ae2f4184a8564272bfb41a21,

title = "Connexin hemichannels influence genetically determined inflammatory and hyperproliferative skin diseases",

abstract = "Connexin mutations underlie numerous human genetic diseases. Several connexin genes have been linked to skin diseases, and mechanistic studies have indicated that a gain of abnormal channel function may be responsible for pathology. The topical accessibility of the epidermal connexins, the existence of several mouse models of human skin disease, and the ongoing identification of pharmacological inhibitors targeting connexins provide an opportunity to test new therapeutic approaches.",

keywords = "Connexin, Gap junctions, Genetic disease, Inflammation, Inhibitor, KID syndrome, Skin",

author = "Levit, \{Noah A.\} and White, \{Thomas W.\}",

note = "Publisher Copyright: {\textcopyright} 2015 Elsevier Ltd.",

year = "2015",

month = jul,

day = "30",

doi = "10.1016/j.phrs.2015.07.015",

language = "English",

volume = "99",

pages = "337--343",

journal = "Pharmacological Research",

issn = "1043-6618",

}

TY - JOUR

T1 - Connexin hemichannels influence genetically determined inflammatory and hyperproliferative skin diseases

AU - Levit, Noah A.

AU - White, Thomas W.

PY - 2015/7/30

Y1 - 2015/7/30

N2 - Connexin mutations underlie numerous human genetic diseases. Several connexin genes have been linked to skin diseases, and mechanistic studies have indicated that a gain of abnormal channel function may be responsible for pathology. The topical accessibility of the epidermal connexins, the existence of several mouse models of human skin disease, and the ongoing identification of pharmacological inhibitors targeting connexins provide an opportunity to test new therapeutic approaches.

AB - Connexin mutations underlie numerous human genetic diseases. Several connexin genes have been linked to skin diseases, and mechanistic studies have indicated that a gain of abnormal channel function may be responsible for pathology. The topical accessibility of the epidermal connexins, the existence of several mouse models of human skin disease, and the ongoing identification of pharmacological inhibitors targeting connexins provide an opportunity to test new therapeutic approaches.

KW - Connexin

KW - Gap junctions

KW - Genetic disease

KW - Inflammation

KW - Inhibitor

KW - KID syndrome

KW - Skin

UR - https://www.scopus.com/pages/publications/84938375875

U2 - 10.1016/j.phrs.2015.07.015

DO - 10.1016/j.phrs.2015.07.015

M3 - Article

C2 - 26211951

AN - SCOPUS:84938375875

SN - 1043-6618

VL - 99

SP - 337

EP - 343

JO - Pharmacological Research

JF - Pharmacological Research

ER -

Connexin hemichannels influence genetically determined inflammatory and hyperproliferative skin diseases

Abstract

Keywords

Access to Document

Other files and links

Fingerprint

Cite this