PMID- 10852107
OWN - NLM
STAT- MEDLINE
DCOM- 20001004
LR  - 20181113
IS  - 0257-277X (Print)
IS  - 0257-277X (Linking)
VI  - 21
IP  - 2-3
DP  - 2000
TI  - Rho GTPase signaling in inflammation and transformation.
PG  - 103-9
AB  - Intracellular Rho GTPases provide an important regulatory mechanism to connect 
      cell-surface-generated signals with the nucleus. By cycling between the active 
      (guanosine 5'-triphosphate [GTP]) and inactive (guanosine 5'-diphosphate) state, 
      these GTP-binding proteins control cellular functions ranging from dynamic actin 
      remodeling and activation of transcription factors to cell-cycle progression and 
      cellular transformation. Their contribution to these very diverse processes makes 
      them an essential part of cell movement, growth, and apoptosis. Upstream 
      regulatory mechanisms, as well as a variety of downstream effector molecules, 
      enable Rho GTPases to act in a specific, orchestrated manner, dictating cellular 
      responses. In this article, I review my laboratory's work centering on the goal 
      of determining how specificity in intracellular signaling is achieved and 
      identifying molecular mechanisms of Rho GTPase-mediated processes in innate 
      immune and transformed cells.
FAU - Knaus, U G
AU  - Knaus UG
AD  - Department of Immunology, The Scripps Research Institute, La Jolla, CA 92037, 
      USA. uknaus@scripps.edu
LA  - eng
PT  - Journal Article
PT  - Review
PL  - United States
TA  - Immunol Res
JT  - Immunologic research
JID - 8611087
RN  - EC 3.6.5.2 (rho GTP-Binding Proteins)
SB  - IM
MH  - Animals
MH  - Humans
MH  - *Immunity, Innate
MH  - Inflammation/immunology
MH  - Signal Transduction/*immunology
MH  - rho GTP-Binding Proteins/*immunology
RF  - 33
EDAT- 2000/06/14 09:00
MHDA- 2000/10/07 11:01
CRDT- 2000/06/14 09:00
PHST- 2000/06/14 09:00 [pubmed]
PHST- 2000/10/07 11:01 [medline]
PHST- 2000/06/14 09:00 [entrez]
AID - IR:21:2-3:103 [pii]
AID - 10.1385/IR:21:2-3:103 [doi]
PST - ppublish
SO  - Immunol Res. 2000;21(2-3):103-9. doi: 10.1385/IR:21:2-3:103.