PMID- 10559204
OWN - NLM
STAT- MEDLINE
DCOM- 19991214
LR  - 20190508
IS  - 0021-9258 (Print)
IS  - 0021-9258 (Linking)
VI  - 274
IP  - 47
DP  - 1999 Nov 19
TI  - Human JIK, a novel member of the STE20 kinase family that inhibits JNK and is
      negatively regulated by epidermal growth factor.
PG  - 33287-95
AB  - Mammalian members related to Saccharomyces cerevisiae serine/threonine kinase
      STE20 can be divided into two subfamilies based on their structure and function. 
      The PAK subfamily is characterized by an N-terminal p21-binding domain (also
      known as CRIB domain), a C-terminal kinase domain, and is regulated by the small 
      GTP-binding proteins Rac1 and Cdc42Hs. The second group is represented by the
      GCK-like members, which contain an N-terminal catalytic domain and lack the
      p21-binding domain. Some of them have been demonstrated to induce c-Jun
      N-terminal kinase/stress-activated protein kinase (JNK/SAPK) cascade, while
      others have been shown to be activated by a subset of stress conditions or
      apoptotic agents, although little is known about their specific function. Here,
      we have identified a novel human STE20-related serine/threonine kinase, belonging
      to the GCK-like subfamily. This kinase does not induce the JNK/SAPK pathway, but,
      instead, inhibits the basal activity of JNK/SAPK, and diminishes its activation
      in response to human epidermal growth factor (EGF). Therefore, we designated this
      molecule JIK for JNK/SAPK-inhibitory kinase. The inhibition of JNK/SAPK signaling
      pathway by JIK was found to occur between the EGF receptor and the small
      GTP-binding proteins Rac1 and Cdc42Hs. In contrast, JIK does not activate nor
      does it inhibit ERK2, ERK6, p38, or ERK5. Furthermore, JIK kinase activity is not
      modulated by any exogenous stimuli, but, interestingly, it is dramatically
      decreased upon EGF receptor activation. Thus, JIK might represent the first
      member of the STE20 kinase family whose activity can be negatively regulated by
      tyrosine kinase receptors, and whose downstream targets inhibit, rather than
      enhance, JNK/SAPK activation.
FAU - Tassi, E
AU  - Tassi E
AD  - Oral and Pharyngeal Cancer Branch, NIDCR, National Institutes of Health,
      Bethesda, Maryland 20892-4330, USA.
FAU - Biesova, Z
AU  - Biesova Z
FAU - Di Fiore, P P
AU  - Di Fiore PP
FAU - Gutkind, J S
AU  - Gutkind JS
FAU - Wong, W T
AU  - Wong WT
LA  - eng
SI  - GENBANK/AF179867
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Biol Chem
JT  - The Journal of biological chemistry
JID - 2985121R
RN  - 0 (DNA Primers)
RN  - 0 (DNA, Complementary)
RN  - 0 (Intracellular Signaling Peptides and Proteins)
RN  - 0 (Nerve Tissue Proteins)
RN  - 0 (RNA, Messenger)
RN  - 0 (Saccharomyces cerevisiae Proteins)
RN  - 62229-50-9 (Epidermal Growth Factor)
RN  - 6C74YM2NGI (Anisomycin)
RN  - EC 2.7.1.- (STK24 protein, human)
RN  - EC 2.7.11.1 (Protein-Serine-Threonine Kinases)
RN  - EC 2.7.11.24 (JNK Mitogen-Activated Protein Kinases)
RN  - EC 2.7.11.24 (Mitogen-Activated Protein Kinases)
RN  - EC 2.7.11.25 (MAP Kinase Kinase Kinases)
RN  - EC 2.7.11.25 (STE20 protein, S cerevisiae)
SB  - IM
MH  - 3T3 Cells
MH  - Amino Acid Sequence
MH  - Animals
MH  - Anisomycin/pharmacology
MH  - Base Sequence
MH  - COS Cells
MH  - DNA Primers
MH  - DNA, Complementary
MH  - Epidermal Growth Factor/*pharmacology
MH  - Gene Expression Regulation
MH  - Humans
MH  - Intracellular Signaling Peptides and Proteins
MH  - JNK Mitogen-Activated Protein Kinases
MH  - MAP Kinase Kinase Kinases
MH  - Mice
MH  - Mitogen-Activated Protein Kinases/*antagonists & inhibitors
MH  - Molecular Sequence Data
MH  - *Nerve Tissue Proteins
MH  - Protein-Serine-Threonine Kinases/chemistry/genetics/*metabolism
MH  - RNA, Messenger/genetics
MH  - *Saccharomyces cerevisiae Proteins
MH  - Sequence Homology, Amino Acid
MH  - Ultraviolet Rays
EDAT- 1999/11/24 00:00
MHDA- 1999/11/24 00:01
CRDT- 1999/11/24 00:00
PHST- 1999/11/24 00:00 [pubmed]
PHST- 1999/11/24 00:01 [medline]
PHST- 1999/11/24 00:00 [entrez]
AID - 10.1074/jbc.274.47.33287 [doi]
PST - ppublish
SO  - J Biol Chem. 1999 Nov 19;274(47):33287-95. doi: 10.1074/jbc.274.47.33287.