Details of Protein

General Information of Protein (ID: PRT01261)
Name Extracellular signal-regulated kinase 2 (ERK2)
Synonyms   Click to Show/Hide Synonyms of This Protein
MAP kinase 1; MAPK 1; ERT1; Extracellular signal-regulated kinase 2; ERK-2; MAP kinase isoform p42; p42-MAPK; Mitogen-activated protein kinase 2; MAP kinase 2; MAPK 2; Mapk1; Erk2; Mapk; Prkm1
Gene Name Mapk1 Gene ID
116590
UniProt ID
P63086
Family Transferases (EC 2)
EC Number   EC: 2.7.11.24  (Click to Show/Hide the Complete EC Tree)
Transferase
Kinase
Protein-serine/threonine kinases
EC: 2.7.11.24
  Click to Show/Hide the Molecular/Functional Data (Sequence/Structure/Function) of This Protein
Sequence
MAAAAAAGPEMVRGQVFDVGPRYTNLSYIGEGAYGMVCSAYDNLNKVRVAIKKISPFEHQ
TYCQRTLREIKILLRFRHENIIGINDIIRAPTIEQMKDVYIVQDLMETDLYKLLKTQHLS
NDHICYFLYQILRGLKYIHSANVLHRDLKPSNLLLNTTCDLKICDFGLARVADPDHDHTG
FLTEYVATRWYRAPEIMLNSKGYTKSIDIWSVGCILAEMLSNRPIFPGKHYLDQLNHILG
ILGSPSQEDLNCIINLKARNYLLSLPHKNKVPWNRLFPNADSKALDLLDKMLTFNPHKRI
EVEQALAHPYLEQYYDPSDEPIAEAPFKFDMELDDLPKEKLKELIFEETARFQPGYRS
Structure
1ERK ; 1GOL ; 2ERK ; 2FYS ; 2GPH ; 2Z7L ; 3C9W ; 3ERK ; 3O71 ; 3QYW ; 3QYZ ; 3R63 ; 3ZU7 ; 3ZUV ; 4ERK ; 4GSB ; 4GT3 ; 4GVA ; 4I5H ; 4N4S ; 4QYY ; 4S2Z ; 4S30 ; 4S31 ; 4S32 ; 4S33 ; 4S34 ; 4XNE ; 4XOY ; 4XOZ ; 4XP0 ; 4XP2 ; 4XP3 ; 4XRJ ; 4XRL ; 5HD4 ; 5HD7 ; 5KE0 ; 5U6I ; 5UMO ; 6CPW ; 6DCG ; 6FI3 ; 6FI6 ; 6FJ0 ; 6FJB ; 6FJZ ; 6FLE ; 6FLV ; 6FMA ; 6FN5 ; 6FQ7 ; 6FR1 ; 6FRP ; 6FXV ; 6OPK ; 6OT6 ; 6OTS ; 6RFO ; 6RFP
Function Serine/threonine kinase which acts as an essential component of the MAP kinase signal transduction pathway. MAPK1/ERK2 and MAPK3/ERK1 are the 2 MAPKs which play an important role in the MAPK/ERK cascade. They participate also in a signaling cascade initiated by activated KIT and KITLG/SCF. Depending on the cellular context, the MAPK/ERK cascade mediates diverse biological functions such as cell growth, adhesion, survival and differentiation through the regulation of transcription, translation, cytoskeletal rearrangements. The MAPK/ERK cascade plays also a role in initiation and regulation of meiosis, mitosis, and postmitotic functions in differentiated cells by phosphorylating a number of transcription factors. About 160 substrates have already been discovered for ERKs. Many of these substrates are localized in the nucleus, and seem to participate in the regulation of transcription upon stimulation. However, other substrates are found in the cytosol as well as in other cellular organelles, and those are responsible for processes such as translation, mitosis and apoptosis. Moreover, the MAPK/ERK cascade is also involved in the regulation of the endosomal dynamics, including lysosome processing and endosome cycling through the perinuclear recycling compartment (PNRC); as well as in the fragmentation of the Golgi apparatus during mitosis. The substrates include transcription factors (such as ATF2, BCL6, ELK1, ERF, FOS, HSF4 or SPZ1), cytoskeletal elements (such as CANX, CTTN, GJA1, MAP2, MAPT, PXN, SORBS3 or STMN1), regulators of apoptosis (such as BAD, BTG2, CASP9, DAPK1, IER3, MCL1 or PPARG), regulators of translation (such as EIF4EBP1) and a variety of other signaling-related molecules (like ARHGEF2, DCC, FRS2 or GRB10). Protein kinases (such as RAF1, RPS6KA1/RSK1, RPS6KA3/RSK2, RPS6KA2/RSK3, RPS6KA6/RSK4, SYK, MKNK1/MNK1, MKNK2/MNK2, RPS6KA5/MSK1, RPS6KA4/MSK2, MAPKAPK3 or MAPKAPK5) and phosphatases (such as DUSP1, DUSP4, DUSP6 or DUSP16) are other substrates which enable the propagation the MAPK/ERK signal to additional cytosolic and nuclear targets, thereby extending the specificity of the cascade. Mediates phosphorylation of TPR in respons to EGF stimulation. May play a role in the spindle assembly checkpoint. Phosphorylates PML and promotes its interaction with PIN1, leading to PML degradation. Phosphorylates CDK2AP2.; Acts as a transcriptional repressor. Binds to a [GC]AAA[GC] consensus sequence. Repress the expression of interferon gamma-induced genes. Seems to bind to the promoter of CCL5, DMP1, IFIH1, IFITM1, IRF7, IRF9, LAMP3, OAS1, OAS2, OAS3 and STAT1. Transcriptional activity is independent of kinase activity.
Regulatory Network
Full List of Metabolite(s) Regulating This Protein
      Lipids and lipid-like molecules
            LysoPS(18:0/0:0) Click to Show/Hide the Full List of Regulating Pair(s):   1 Pair(s)
               Detailed Information Metabo  Info click to show the details of this metabolite
               Regulating Pair Experim Info click to show the details of experiment for validating this pair [1]
                      Introduced Variation LysoPS(18:0/0:0) addition (8.3310^-4 hours)
                      Induced Change MAPK1 protein phosphorylation levels: increase
                      Summary Introduced Variation         Induced Change 
                      Disease Status Anaphylaxis [ICD-11: 4A84]
                      Details It is reported that lysoPS(18:0/0:0) addition causes the increase of MAPK1 protein phosphorylation compared with control group.
      Organic acids and derivatives
            Glutamine Click to Show/Hide the Full List of Regulating Pair(s):   1 Pair(s)
               Detailed Information Metabo  Info click to show the details of this metabolite
               Regulating Pair Experim Info click to show the details of experiment for validating this pair [2]
                      Introduced Variation Glutamine addition (6 hours)
                      Induced Change MAPK1 protein phosphorylation levels: decrease
                      Summary Introduced Variation         Induced Change 
                      Disease Status Sepsis [ICD-11: 1G40]
                      Details It is reported that glutamine addition causes the decrease of MAPK1 protein phosphorylation compared with control group.
References
1 Identification of a lysophosphatidylserine receptor on mast cells. Biochem Biophys Res Commun. 2006 Mar 24;341(4):1078-87.
2 GLUTAMINE PREVENTS ACTIVATION OF NF-kappaB AND STRESS KINASE PATHWAYS, ATTENUATES INFLAMMATORY CYTOKINE RELEASE, AND PREVENTS ACUTE RESPIRATORY DISTRESS SYNDROME (ARDS) FOLLOWING SEPSIS. Shock. 2005 Dec;24(6):583-9.

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