PMID- 37082594
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20230422
IS  - 2667-1603 (Electronic)
IS  - 2667-1603 (Linking)
VI  - 2
DP  - 2022
TI  - A global analysis on the differential regulation of RNA binding proteins (RBPs) 
      by TNF-alpha as potential modulators of metabolic syndromes.
PG  - 100037
LID - 10.1016/j.bbadva.2021.100037 [doi]
LID - 100037
AB  - Metabolic syndrome (MetS) is associated with a group of conditions, which 
      enhances the risk of diabetes, heart diseases and stroke in the affected 
      individuals. Earlier reports from our lab have shown that Tumor necrosis factor-alpha 
      (TNF-alpha) significantly modulates the expression of 56 genes at the alternative 
      splicing level which are involved in various signaling and metabolic pathways 
      (MetS genes) connected to MetS. These MetS genes were predicted to interact with 
      various RNA-binding proteins (RBPs) when exposed to TNF-alpha, resulting changes in 
      their alternative splicing patterns. Here we are presenting data of an RNA-Seq 
      analysis, which identified 1218 unique, and significantly regulated genes by 
      TNF-alpha, 15% of which are RBPs . Among the 1218 genes, 204 genes have been 
      identified as MetS genes by the ingenuity pathway analysis, and 10% of the MetS 
      genes are found as RBPs. Our results also show that TNF-alpha changes the 
      phosphorylation status of certain RBPs such as SR proteins, crucial players in 
      alternative splicing, possibly via changing the activation status of certain 
      upstream signaling molecules which also act as upstream kinases for these 
      proteins. Taken together, these findings suggest that TNF-alpha influences the 
      regulation of the RBPs at the various levels for their expression, which may lead 
      to the alteration of the splicing pattern of the MetS genes. MetS genes acting as 
      RBPs and are modulated by TNF-alpha, predict the existence of highly interconnected 
      mechanisms which require further analysis to understand their dual roles on the 
      onset of these diseases.
CI  - (c) 2021 The Authors.
FAU - Louis, Jiss Maria
AU  - Louis JM
AD  - Department of Biological Sciences, BITS Pilani K K Birla Goa campus, Zuarinagar, 
      Goa 403726, India.
FAU - Agarwal, Arjun
AU  - Agarwal A
AD  - Department of Computer Science, BITS Pilani K K Birla Goa campus, Zuarinagar, Goa 
      403726, India.
FAU - Mondal, Sukanta
AU  - Mondal S
AD  - Department of Biological Sciences, BITS Pilani K K Birla Goa campus, Zuarinagar, 
      Goa 403726, India.
FAU - Talukdar, Indrani
AU  - Talukdar I
AD  - Department of Biological Sciences, BITS Pilani K K Birla Goa campus, Zuarinagar, 
      Goa 403726, India.
LA  - eng
PT  - Journal Article
DEP - 20211229
PL  - Netherlands
TA  - BBA Adv
JT  - BBA advances
JID - 9918227371406676
PMC - PMC10074950
OTO - NOTNLM
OT  - Gene regulation
OT  - MetS genes
OT  - Metabolic syndromes
OT  - RNA binding proteins
OT  - RNA seq analysis
OT  - TNF-alpha
COIS- The authors declare that they have no known competing financial interests or 
      personal relationships that could have appeared to influence the work reported in 
      this paper.
EDAT- 2021/12/29 00:00
MHDA- 2021/12/29 00:01
PMCR- 2021/12/29
CRDT- 2023/04/21 02:29
PHST- 2021/05/09 00:00 [received]
PHST- 2021/12/12 00:00 [revised]
PHST- 2021/12/15 00:00 [accepted]
PHST- 2021/12/29 00:01 [medline]
PHST- 2021/12/29 00:00 [pubmed]
PHST- 2023/04/21 02:29 [entrez]
PHST- 2021/12/29 00:00 [pmc-release]
AID - S2667-1603(21)00036-3 [pii]
AID - 100037 [pii]
AID - 10.1016/j.bbadva.2021.100037 [doi]
PST - epublish
SO  - BBA Adv. 2021 Dec 29;2:100037. doi: 10.1016/j.bbadva.2021.100037. eCollection 
      2022.