PMID- 30270668
OWN - NLM
STAT- MEDLINE
DCOM- 20200323
LR  - 20211204
IS  - 1744-4160 (Electronic)
IS  - 1381-3455 (Linking)
VI  - 126
IP  - 2
DP  - 2020 May
TI  - Regulation of insulin resistance and glucose metabolism by interaction of PIM 
      kinases and insulin receptor substrates.
PG  - 129-138
LID - 10.1080/13813455.2018.1498903 [doi]
AB  - Insulin resistance is caused by various environmental and genetic factors leading 
      to a number of serious health issues. Due to its multifactorial origin, molecular 
      characterization may provide better tools for its effective treatment. On 
      molecular level, dysregulation of signaling pathway by insulin receptor 
      substrates (IRSs) is one of the most common reasons of this disease. IRSs are 
      regulated by >50 serine/threonine kinases, which may have positive or negative 
      effects on insulin sensitivity. Among these serine/threonine kinases, PIM kinases 
      have garnered much attention as they not only affect insulin sensitivity by 
      phosphorylating IRSs directly and/or indirectly but also alter the activities of 
      their downstream molecules like PI3K, AKT, and mTOR. In this review, interactions 
      of PIM kinases with IRSs and their downstream proteins and their action mechanism 
      in the regulation of insulin resistance are elaborated. Furthermore, this review 
      offers fundamental understandings of the role of PIM kinases in this signaling 
      pathway.
FAU - Aziz, Aziz Ur Rehman
AU  - Aziz AUR
AD  - School of Biomedical Engineering, Dalian University of Technology, Dalian, China.
FAU - Farid, Sumbal
AU  - Farid S
AD  - State Key Laboratory of Fine Chemicals, Dalian University of Technology, Dalian, 
      China.
FAU - Qin, Kairong
AU  - Qin K
AD  - School of Biomedical Engineering, Dalian University of Technology, Dalian, China.
FAU - Wang, Hanqin
AU  - Wang H
AD  - Center for Translational Medicine, Suizhou Hospital, Hubei University of 
      Medicine, Suizhou, China.
FAU - Liu, Bo
AU  - Liu B
AD  - School of Biomedical Engineering, Dalian University of Technology, Dalian, China.
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20180929
PL  - England
TA  - Arch Physiol Biochem
JT  - Archives of physiology and biochemistry
JID - 9510153
RN  - 0 (Antigens, CD)
RN  - 0 (Insulin)
RN  - 0 (Insulin Receptor Substrate Proteins)
RN  - EC 2.7.1.1 (MTOR protein, human)
RN  - EC 2.7.10.1 (INSR protein, human)
RN  - EC 2.7.10.1 (Receptor, Insulin)
RN  - EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
RN  - EC 2.7.11.1 (Proto-Oncogene Proteins c-pim-1)
RN  - EC 2.7.11.1 (TOR Serine-Threonine Kinases)
RN  - EC 2.7.11.1 (proto-oncogene proteins pim)
RN  - IY9XDZ35W2 (Glucose)
SB  - IM
MH  - Animals
MH  - Antigens, CD/*genetics/metabolism
MH  - Gene Expression Regulation
MH  - Glucose/*metabolism
MH  - Humans
MH  - Insulin/genetics/metabolism
MH  - Insulin Receptor Substrate Proteins/*genetics/metabolism
MH  - *Insulin Resistance
MH  - Phosphatidylinositol 3-Kinases/genetics/metabolism
MH  - Phosphorylation
MH  - Proto-Oncogene Proteins c-akt/genetics/metabolism
MH  - Proto-Oncogene Proteins c-pim-1/*genetics/metabolism
MH  - Receptor, Insulin/*genetics/metabolism
MH  - Signal Transduction
MH  - TOR Serine-Threonine Kinases/genetics/metabolism
OTO - NOTNLM
OT  - Insulin receptor substrates
OT  - PI3K
OT  - PIM
OT  - insulin signaling pathways
OT  - mTOR
EDAT- 2018/10/03 06:00
MHDA- 2020/03/24 06:00
CRDT- 2018/10/02 06:00
PHST- 2018/10/03 06:00 [pubmed]
PHST- 2020/03/24 06:00 [medline]
PHST- 2018/10/02 06:00 [entrez]
AID - 10.1080/13813455.2018.1498903 [doi]
PST - ppublish
SO  - Arch Physiol Biochem. 2020 May;126(2):129-138. doi: 
      10.1080/13813455.2018.1498903. Epub 2018 Sep 29.