PMID- 34680077
OWN - NLM
STAT- MEDLINE
DCOM- 20220118
LR  - 20220430
IS  - 2218-273X (Electronic)
IS  - 2218-273X (Linking)
VI  - 11
IP  - 10
DP  - 2021 Oct 2
TI  - Stress Relief Techniques: p38 MAPK Determines the Balance of Cell Cycle and 
      Apoptosis Pathways.
LID - 10.3390/biom11101444 [doi]
LID - 1444
AB  - Protein signaling networks are formed from diverse and inter-connected cell 
      signaling pathways converging into webs of function and regulation. These 
      signaling pathways both receive and conduct molecular messages, often by a series 
      of post-translation modifications such as phosphorylation or through 
      protein-protein interactions via intrinsic motifs. The mitogen activated protein 
      kinases (MAPKs) are components of kinase cascades that transmit signals through 
      phosphorylation. There are several MAPK subfamilies, and one subfamily is the 
      stress-activated protein kinases, which in mammals is the p38 family. The p38 
      enzymes mediate a variety of cellular outcomes including DNA repair, cell 
      survival/cell fate decisions, and cell cycle arrest. The cell cycle is itself a 
      signaling system that precisely controls DNA replication, chromosome segregation, 
      and cellular division. Another indispensable cell function influenced by the p38 
      stress response is programmed cell death (apoptosis). As the regulators of cell 
      survival, the BCL2 family of proteins and their dynamics are exquisitely 
      sensitive to cell stress. The BCL2 family forms a protein-protein interaction 
      network divided into anti-apoptotic and pro-apoptotic members, and the balance of 
      binding between these two sides determines cell survival. Here, we discuss the 
      intersections among the p38 MAPK, cell cycle, and apoptosis signaling pathways.
FAU - Whitaker, Robert H
AU  - Whitaker RH
AUID- ORCID: 0000-0002-9751-0423
AD  - Department of Biochemistry & Biophysics, University of North Carolina at Chapel 
      Hill, Chapel Hill, NC 27599, USA.
FAU - Cook, Jeanette Gowen
AU  - Cook JG
AUID- ORCID: 0000-0003-0849-7405
AD  - Department of Biochemistry & Biophysics, University of North Carolina at Chapel 
      Hill, Chapel Hill, NC 27599, USA.
LA  - eng
GR  - R01GM102413/GM/NIGMS NIH HHS/United States
GR  - R01 GM083024/GM/NIGMS NIH HHS/United States
GR  - T32 CA009156/CA/NCI NIH HHS/United States
GR  - R35GM141833/GM/NIGMS NIH HHS/United States
GR  - T32CA009156/CA/NCI NIH HHS/United States
GR  - R01 GM102413/GM/NIGMS NIH HHS/United States
GR  - R01GM083024/GM/NIGMS NIH HHS/United States
GR  - R35 GM141833/GM/NIGMS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Review
DEP - 20211002
PL  - Switzerland
TA  - Biomolecules
JT  - Biomolecules
JID - 101596414
RN  - 0 (BCL2 protein, human)
RN  - 0 (Proto-Oncogene Proteins c-bcl-2)
RN  - EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases)
SB  - IM
MH  - Apoptosis/*genetics
MH  - Cell Cycle/*genetics
MH  - Cell Cycle Checkpoints/genetics
MH  - DNA Repair/genetics
MH  - Humans
MH  - Phosphorylation/genetics
MH  - Protein Interaction Maps/genetics
MH  - Protein Processing, Post-Translational/genetics
MH  - Proto-Oncogene Proteins c-bcl-2/genetics
MH  - Signal Transduction/genetics
MH  - p38 Mitogen-Activated Protein Kinases/*genetics
PMC - PMC8533283
OTO - NOTNLM
OT  - DNA damage
OT  - apoptosis
OT  - cell cycle
OT  - cell signaling
OT  - cell stress
OT  - chemotherapy
OT  - kinase
OT  - mitosis
OT  - protein networks
COIS- The authors declare no conflict of interest.
EDAT- 2021/10/24 06:00
MHDA- 2022/01/19 06:00
PMCR- 2021/10/02
CRDT- 2021/10/23 01:02
PHST- 2021/07/23 00:00 [received]
PHST- 2021/09/23 00:00 [revised]
PHST- 2021/09/30 00:00 [accepted]
PHST- 2021/10/23 01:02 [entrez]
PHST- 2021/10/24 06:00 [pubmed]
PHST- 2022/01/19 06:00 [medline]
PHST- 2021/10/02 00:00 [pmc-release]
AID - biom11101444 [pii]
AID - biomolecules-11-01444 [pii]
AID - 10.3390/biom11101444 [doi]
PST - epublish
SO  - Biomolecules. 2021 Oct 2;11(10):1444. doi: 10.3390/biom11101444.