PMID- 31867000
OWN - NLM
STAT- MEDLINE
DCOM- 20201110
LR  - 20201110
IS  - 1664-3224 (Electronic)
IS  - 1664-3224 (Linking)
VI  - 10
DP  - 2019
TI  - Arid5a Regulation and the Roles of Arid5a in the Inflammatory Response and 
      Disease.
PG  - 2790
LID - 10.3389/fimmu.2019.02790 [doi]
LID - 2790
AB  - Abnormal gene expression patterns underlie many diseases that represent major 
      public health concerns and robust therapeutic challenges. Posttranscriptional 
      gene regulation by RNA-binding proteins (RBPs) is well-recognized, and the 
      biological functions of RBPs have been implicated in many diseases, such as 
      autoimmune diseases, inflammatory diseases, and cancer. However, a complete 
      understanding of the regulation mediated by several RBPs is lacking. During the 
      past few years, a novel role of AT-rich interactive domain-containing protein 5a 
      (Arid5a) as an RBP is being investigated in the field of immunology owing to 
      binding of Arid5a protein to the 3' untranslated region (UTR) of Il-6 mRNA. 
      Indeed, Arid5a is a dynamic molecule because upon inflammation, it translocates 
      to the cytoplasm and stabilizes a variety of inflammatory mRNA transcripts, 
      including Il-6, Stat3, Ox40, T-bet, and IL-17-induced targets, and contributes to 
      the inflammatory response and a variety of diseases. TLR4-activated NF-kappaB and 
      MAPK pathways are involved in regulating Arid5a expression from synthesis to 
      degradation, and even a slight alteration in these pathways can lead to intense 
      production of inflammatory molecules, such as IL-6, which may further contribute 
      to the development of inflammatory diseases such as sepsis and experimental 
      autoimmune encephalomyelitis. This review highlights the regulation of the Arid5a 
      expression and function. Additionally, recent findings on Arid5a are discussed to 
      further our understanding of this molecule, which may be a promising therapeutic 
      target for inflammatory diseases.
CI  - Copyright (c) 2019 Nyati, Agarwal, Sharma and Kishimoto.
FAU - Nyati, Kishan Kumar
AU  - Nyati KK
AD  - Laboratory of Immune Regulation, Immunology Frontier Research Center, Osaka 
      University, Osaka, Japan.
AD  - Department of Biochemistry, All India Institute of Medical Sciences, Jodhpur, 
      India.
FAU - Agarwal, Riddhi Girdhar
AU  - Agarwal RG
AD  - Department of Biochemistry, All India Institute of Medical Sciences, Jodhpur, 
      India.
FAU - Sharma, Praveen
AU  - Sharma P
AD  - Department of Biochemistry, All India Institute of Medical Sciences, Jodhpur, 
      India.
FAU - Kishimoto, Tadamitsu
AU  - Kishimoto T
AD  - Laboratory of Immune Regulation, Immunology Frontier Research Center, Osaka 
      University, Osaka, Japan.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
DEP - 20191205
PL  - Switzerland
TA  - Front Immunol
JT  - Frontiers in immunology
JID - 101560960
RN  - 0 (ARID5A protein, human)
RN  - 0 (Biomarkers)
RN  - 0 (DNA-Binding Proteins)
RN  - 0 (RNA, Messenger)
RN  - 0 (Toll-Like Receptor 4)
SB  - IM
MH  - Animals
MH  - Biomarkers
MH  - DNA-Binding Proteins/*genetics/*metabolism
MH  - *Disease Susceptibility/immunology
MH  - Gene Expression Profiling
MH  - Humans
MH  - Inflammation/*etiology/*metabolism/pathology/therapy
MH  - RNA Processing, Post-Transcriptional
MH  - RNA Stability
MH  - RNA, Messenger/genetics
MH  - Toll-Like Receptor 4/metabolism
PMC - PMC6906145
OTO - NOTNLM
OT  - Arid5a
OT  - TLR4
OT  - immune regulation
OT  - inflammation
OT  - mRNA stability
OT  - posttranscriptional regulation
EDAT- 2019/12/24 06:00
MHDA- 2020/11/11 06:00
PMCR- 2019/01/01
CRDT- 2019/12/24 06:00
PHST- 2019/07/31 00:00 [received]
PHST- 2019/11/14 00:00 [accepted]
PHST- 2019/12/24 06:00 [entrez]
PHST- 2019/12/24 06:00 [pubmed]
PHST- 2020/11/11 06:00 [medline]
PHST- 2019/01/01 00:00 [pmc-release]
AID - 10.3389/fimmu.2019.02790 [doi]
PST - epublish
SO  - Front Immunol. 2019 Dec 5;10:2790. doi: 10.3389/fimmu.2019.02790. eCollection 
      2019.