State-of-the-Art in STAT Protein

A special issue of Life (ISSN 2075-1729). This special issue belongs to the section "Pharmaceutical Science".

Deadline for manuscript submissions: closed (18 March 2022) | Viewed by 3068

Special Issue Editor

Department of Pharmacology, College of Korean Medicine, Sangji University, Wonju 26339, Gangwon-do, Korea
Interests: benign prostatic hyperplasia; inflammation; allergy; atopic dermatitis; obesity; pharmacology; herbal medicine; natural product

Special Issue Information

Dear Colleagues,

The signal transducer and activator of transcription (STAT) protein family consists of latent cytoplasmic transcription factors. Since the first discovery of STAT in the 1990s, its structure, activation, function, and regulation have been investigated in a great deal of pathophysiological situations. As the intracellular transcription factors, they mediate a number of areas of physiologic cell processes, including cellular immunity, proliferation, differentiation, and apoptosis. Seven STAT genes in mammalian genomes have been identified so far; namely STAT1, STAT2, STAT3, STAT4, STAT5A, STAT5B, and STAT6. Each of them plays a different role in the consideration of diverse extracellular signaling proteins which primarily alter gene transcription in the effector cells. Furthermore, the STAT pathway is connected to the Janus kinases (JAK) family protein, and able to integrate inputs from various signaling pathways. This is why STAT is a potential key mediator in diseases.

This Special Issue aims to gather contributions on review and primary research articles, aiming to update and advance the current knowledge on STAT proteins. The suggested potential topics are not restricted to STAT itself, but also its related protein or involved pathways. Your diverse works will help to clarify the STAT protein, forming numerous insights into many diseases.

Dr. Hyo Jin An
Guest Editor

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Keywords

  • STAT
  • inflammation
  • immunology
  • apoptosis
  • angiogenesis

Published Papers (1 paper)

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Research

11 pages, 5317 KiB  
Article
Euphorbia hirta Leaf Ethanol Extract Suppresses TNF-α/IFN-γ-Induced Inflammatory Response via Down-Regulating JNK or STAT1/3 Pathways in Human Keratinocytes
by Tae-Young Gil, Sung-Chul Kang, Bo-Ram Jin and Hyo-Jin An
Life 2022, 12(4), 589; https://doi.org/10.3390/life12040589 - 15 Apr 2022
Cited by 1 | Viewed by 2580
Abstract
Skin inflammation may cause allergic diseases such as allergic rhinitis, asthma, and atopic dermatitis. Euphorbia hirta (E. hirta) is a member of the Euphorbiaceae family and is well-known for its anti-asthma effects. E. hirta has traditionally been used to treat respiratory [...] Read more.
Skin inflammation may cause allergic diseases such as allergic rhinitis, asthma, and atopic dermatitis. Euphorbia hirta (E. hirta) is a member of the Euphorbiaceae family and is well-known for its anti-asthma effects. E. hirta has traditionally been used to treat respiratory ailments, dysentery, jaundice, and digestive problems. However, its effects on skin inflammation remain unclear. Here, we determined the effects of 70% ethanol extract of E. hirta leaves (ELE) in vitro using human keratinocyte HaCaT cells, which constitute most epidermal skin cells. We determined the inhibitory effects of ELE on the inflammation caused by tumor necrosis factor (TNF)-α/interferon (IFN)-γ in keratinocytes using ELISA, immunoblotting, and qRT-PCR assay. ELE was found to reduce the production and mRNA expression of pro-inflammatory cytokines such as TNF-α or interleukin-6 and the expression of various proteins, including signal transducers, activators of transcription 1/3, and mitogen-activated protein kinase. Expression levels of these proteins were found to be upregulated in the TNF-α/IFN-γ-stimulated condition and downregulated by ELE treatment. These results indicate that ELE protects HaCaT cells against TNF-α/IFN-γ-induced skin inflammation. Full article
(This article belongs to the Special Issue State-of-the-Art in STAT Protein)
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