PMID- 35174412
OWN - NLM
STAT- MEDLINE
DCOM- 20220510
LR  - 20220623
IS  - 1432-1211 (Electronic)
IS  - 0093-7711 (Linking)
VI  - 74
IP  - 3
DP  - 2022 Jun
TI  - The S100A7 nuclear interactors in autoimmune diseases: a coevolutionary study in 
      mammals.
PG  - 271-284
LID - 10.1007/s00251-022-01256-7 [doi]
AB  - S100A7, a member of the S100A family of Ca(2+)-binding proteins, is considered a 
      key effector in immune response. In particular, S100A7 dysregulation has been 
      associated with several diseases, including autoimmune disorders. At the nuclear 
      level, S100A7 interacts with several protein-binding partners which are involved 
      in transcriptional regulation and DNA repair. By using the BioGRID and GAAD 
      databases, S100A7 nuclear interactors with a putative involvement in autoimmune 
      diseases were retrieved. We selected fatty acid-binding protein 5 (FABP5), 
      autoimmune regulator (AIRE), cystic fibrosis transmembrane conductance regulator 
      (CFTR), chromodomain helicase DNA-binding protein 4 (CHD4), epidermal growth 
      factor receptor (EGFR), estrogen receptor 1 (ESR1), histone deacetylase 2 
      (HDAC2), v-myc avian myelocytomatosis viral oncogene homolog (MYC), protection of 
      telomeres protein 1 (POT1), telomeric repeat-binding factor (NIMA-interacting) 1 
      (TERF1), telomeric repeat-binding factor 2 (TERF2), and Zic family member 1 
      (ZIC1). Linear correlation coefficients between interprotein distances were 
      calculated with MirrorTree. Coevolution clusters were also identified with the 
      use of a recent version of the Blocks in Sequences (BIS2) algorithm implemented 
      in the BIS2Analyzer web server. Analysis of pair positions identified 
      interprotein coevolving clusters between S100A7 and the binding partners CFTR and 
      TERF1. Such findings could guide further analysis to better elucidate the 
      function of S100A7 and its binding partners and to design drugs targeting for 
      these molecules in autoimmune diseases.
CI  - (c) 2022. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, 
      part of Springer Nature.
FAU - D'Amico, Fabio
AU  - D'Amico F
AUID- ORCID: 0000-0002-5551-8291
AD  - Department of Biomedical and Biotechnological Sciences, University of Catania, 
      via Santa Sofia 97, Catania, 95123, Italy. f.damico@unict.it.
FAU - Skarmoutsou, Evangelia
AU  - Skarmoutsou E
AD  - , Catania, Italy.
FAU - Libra, Massimo
AU  - Libra M
AD  - Department of Biomedical and Biotechnological Sciences, University of Catania, 
      via Santa Sofia 97, Catania, 95123, Italy.
LA  - eng
PT  - Journal Article
DEP - 20220216
PL  - United States
TA  - Immunogenetics
JT  - Immunogenetics
JID - 0420404
RN  - 0 (DNA-Binding Proteins)
RN  - 126880-72-6 (Cystic Fibrosis Transmembrane Conductance Regulator)
SB  - IM
MH  - Animals
MH  - *Autoimmune Diseases/genetics
MH  - *Cystic Fibrosis Transmembrane Conductance Regulator
MH  - DNA-Binding Proteins
MH  - Mammals/genetics
OTO - NOTNLM
OT  - Autoimmune diseases
OT  - Cell nucleus
OT  - Coevolution
OT  - S100A7
EDAT- 2022/02/18 06:00
MHDA- 2022/05/11 06:00
CRDT- 2022/02/17 05:39
PHST- 2021/11/21 00:00 [received]
PHST- 2022/02/10 00:00 [accepted]
PHST- 2022/02/18 06:00 [pubmed]
PHST- 2022/05/11 06:00 [medline]
PHST- 2022/02/17 05:39 [entrez]
AID - 10.1007/s00251-022-01256-7 [pii]
AID - 10.1007/s00251-022-01256-7 [doi]
PST - ppublish
SO  - Immunogenetics. 2022 Jun;74(3):271-284. doi: 10.1007/s00251-022-01256-7. Epub 
      2022 Feb 16.