PMID- 10611248
OWN - NLM
STAT- MEDLINE
DCOM- 20000127
LR  - 20190508
IS  - 0270-7306 (Print)
IS  - 0270-7306 (Linking)
VI  - 20
IP  - 2
DP  - 2000 Jan
TI  - Gastric hyperplasia in mice lacking the putative Cdc42 effector IQGAP1.
PG  - 697-701
AB  - Human IQGAP1 is a widely expressed 190-kDa Cdc42-, Rac1-, and calmodulin-binding 
      protein that interacts with F-actin in vivo and that can cross-link F-actin
      microfilaments in vitro. Recent results have implicated IQGAP1 as a component of 
      pathways via which Cdc42 or Rac1 modulates cadherin-based cell adhesion (S.
      Kuroda et al., Science 281:832-835, 1998), whereas yeast IQGAP-related proteins
      have been found to play essential roles during cytokinesis. To identify critical 
      in vivo functions of IQGAP1, we generated deficient mice by gene targeting. We
      demonstrate that IQGAP1 null mutants arise at normal frequency and show no
      obvious defects during development or for most of their adult life. Loss of
      IQGAP1 also does not affect tumor development or tumor progression, but mutant
      mice exhibit a significant (P < 0.0001) increase in late-onset gastric
      hyperplasia relative to wild-type animals of the same genetic background. While
      we cannot exclude that functional redundancy with IQGAP2 contributes to the lack 
      of developmental phenotypes, the restricted expression pattern of IQGAP2 is not
      obviously altered in adult IQGAP1 mutant mice. Thus, IQGAP1 does not serve any
      essential nonredundant functions during murine development but may serve to
      maintain the integrity of the gastric mucosa in older animals.
FAU - Li, S
AU  - Li S
AD  - Massachusetts General Hospital Cancer Center, Harvard Medical School,
      Charlestown, Massachusetts 02129, USA.
FAU - Wang, Q
AU  - Wang Q
FAU - Chakladar, A
AU  - Chakladar A
FAU - Bronson, R T
AU  - Bronson RT
FAU - Bernards, A
AU  - Bernards A
LA  - eng
GR  - CA70294/CA/NCI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Mol Cell Biol
JT  - Molecular and cellular biology
JID - 8109087
RN  - 0 (Cadherins)
RN  - 0 (Carrier Proteins)
RN  - 0 (IQ motif containing GTPase activating protein 1)
RN  - 0 (Iqgap2 protein, mouse)
RN  - 0 (RNA, Messenger)
RN  - 0 (ras GTPase-Activating Proteins)
RN  - EC 3.6.5.2 (cdc42 GTP-Binding Protein)
SB  - IM
MH  - Amino Acid Sequence
MH  - Animals
MH  - Cadherins/physiology
MH  - Carrier Proteins/genetics/*metabolism
MH  - Exons/genetics
MH  - Female
MH  - Gastric Mucosa/metabolism
MH  - Gene Deletion
MH  - Gene Expression Profiling
MH  - Genes, Essential/genetics
MH  - Genotype
MH  - Hyperplasia/genetics/pathology
MH  - Male
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Mice, Knockout
MH  - Molecular Sequence Data
MH  - Neoplasms/metabolism/pathology
MH  - Phenotype
MH  - RNA, Messenger/analysis/genetics
MH  - Sequence Homology, Amino Acid
MH  - Stomach/*pathology
MH  - cdc42 GTP-Binding Protein/*physiology
MH  - *ras GTPase-Activating Proteins
PMC - PMC85173
EDAT- 1999/12/28 00:00
MHDA- 1999/12/28 00:01
CRDT- 1999/12/28 00:00
PHST- 1999/12/28 00:00 [pubmed]
PHST- 1999/12/28 00:01 [medline]
PHST- 1999/12/28 00:00 [entrez]
AID - 10.1128/mcb.20.2.697-701.2000 [doi]
PST - ppublish
SO  - Mol Cell Biol. 2000 Jan;20(2):697-701. doi: 10.1128/mcb.20.2.697-701.2000.