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 3622

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

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Life is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • STAT
  • inflammation
  • immunology
  • apoptosis
  • angiogenesis

Benefits of Publishing in a Special Issue

  • Ease of navigation: Grouping papers by topic helps scholars navigate broad scope journals more efficiently.
  • Greater discoverability: Special Issues support the reach and impact of scientific research. Articles in Special Issues are more discoverable and cited more frequently.
  • Expansion of research network: Special Issues facilitate connections among authors, fostering scientific collaborations.
  • External promotion: Articles in Special Issues are often promoted through the journal's social media, increasing their visibility.
  • e-Book format: Special Issues with more than 10 articles can be published as dedicated e-books, ensuring wide and rapid dissemination.

Further information on MDPI's Special Issue polices can be found here.

Published Papers (1 paper)

Order results
Result details
Select all
Export citation of selected articles as:

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 3 | Viewed by 3066
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)
Show Figures

Graphical abstract

Back to TopTop