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Query: UNIPROT:P06889 (Mol)
 630,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Some ants have an extraordinary unicolonial social organization, whereby individuals mix freely among physically separated nests. Recently, it was shown that the European population of Linepithema humile consisted of two enormous unicolonial supercolonies. Workers of the same supercolony are never aggressive to each other. In contrast, aggressiveness is invariably high between workers from different supercolonies. Here we investigated whether gene flow occurs between two supercolonies. We identified a contact zone in which we sampled 46 nests. For each nest, aggression tests were conducted against workers from reference nests from both supercolonies. Workers were always very aggressive towards workers of one of the supercolonies but not to workers of the other. Thus, all nests could be clearly assigned to one of the two supercolonies. For 22 of the 46 nests, we genotyped 15-16 workers at five microsatellite loci. A four-level hierarchical analysis of variance revealed very strong genetic differentiation between the two supercolonies (F(SUPERCOLONY-TOTAL) = 0.541) and low differentiation between sectors (i.e. group of nests connected together with trails) within supercolonies (F(SECTOR-SUPERCOLONY) = 0.064). The very high differentiation between the two supercolonies indicates a lack of ongoing gene flow, a conclusion further bolstered by the finding that the two supercolonies share no common alleles at two of the five microsatellite loci. A Bayesian clustering method also revealed the occurrence of two distinct clusters. These clusters exactly match the grouping obtained by aggression tests. None of the 332 genotyped individuals were admixed despite the fact that some nests of the two supercolonies were separated by less than 30 m. These results demonstrate that the two supercolonies have completely separate gene pools.
Mol Ecol 2005 Feb
PMID:Multilevel genetic analyses of two European supercolonies of the Argentine ant, Linepithema humile. 1566 Sep 48

A negative correlation was observed between the aggressiveness of several Erwinia chrysanthemi strains on potato tuber and their osmotic tolerance. The disruption of the ousA gene encoding the major osmoprotectant uptake system highly enhanced bacterial virulence on potato tubers. The ousA disruption also increased the maceration efficiency on potato tubers under anaerobic conditions. In the absence of oxygen, pectate lyase (Pel) production was significantly higher in the tissue macerated with the ousA- strain than with the wild type. Oxygen content is significantly different between infected and healthy tissues; therefore, ousA may be a contributory factor in the infection progression within the host. In minimal medium, ousA disruption enhanced Pel production and pelE expression only under micro-aerobiosis conditions. The effect on Pel was reversed by reintroduction of the ousA gene. The osmoprotectectants glycine betaine, proline betaine, and pipecolic acid are known to be taken up via OusA and to have an inhibitory effect on Pel production. However, their effects on Pel activity were not (glycine betaine) or only weakly (proline and pipecolic acid) affected by ousA disruption. Furthermore, no correlation was observed between their effects on Pel activities and their osmoprotection efficacies. The results demonstrate a relationship between E. chrysanthemi pathogenicity factors and the activity of ousA under low oxygen status. The evidence indicates that ousA and osmoprotectant effects on Pel are not linked to osmoregulation and that complex regulations exist between Pel production, ousA, and osmoprotection via compounds liberated during the plant infection.
Mol Plant Microbe Interact 2005 Feb
PMID:Mutations of ousA alter the virulence of Erwinia chrysanthemi. 1572 84

Many checkpoint proteins that are involved in the control of the cell cycle and apoptosis have been investigated, but only a few studies have evaluated the prognostic significance of multiple factors only in rectal carcinomas. The aim of this study was to determine the role of p53, p21, and p27 protein expression as a prognostic factor in rectal carcinomas. Formalin-fixed, paraffin-embedded tissue blocks from 45 rectal adenocarcinomas with appropriate clinical and prognostic data were examined. The standard streptavidin-biotin immunoperoxidase method was used for immunostaining with p53 protein, p21 WAF1/Cip1 protein, and p27 Kip1 protein. The extent of positive p53, p21, and p27 staining was graded semiquantitatively. The clinicopathologic and prognostic features were statistically analyzed. No significant association was found between p53 status and p21 or p27 protein expression (chi2 test, P=0.42 and P=0.18 respectively). There was no correlation between the expressions of p53, p21, and p27, and conventional clinicopathologic features. The mean time interval to recurrence was 25.7+/-24.7 months (range, 0-54 months). p53, p21, and p27 expression was not associated significantly with recurrence and distant metastasis. However, a significant relationship was found between the expression of p27 protein and hepatic metastasis (independent samples t-test, P=0.007). The authors concluded that p53, p27, and p21 protein expression was not related to the clinicopathologic parameters, tumor aggressiveness, metastatic potential, and survival in rectal carcinomas. Further studies are needed to evaluate the predictors of outcome in rectal cancer, considering a variety of prognosticators.
Appl Immunohistochem Mol Morphol 2005 Mar
PMID:The clinical significance of p53, p21, and p27 expressions in rectal carcinoma. 1572 92

The transcriptional regulating protein of 132 kDa (TReP-132) has been identified in steroidogenic tissues, where it acts as a coactivator of steroidogenic factor 1 (SF-1). We show here that TReP-132 plays a role in the control of cell proliferation. In human HeLa cells, TReP-132 knockdown by using small interfering RNA resulted in increased G(1)-->S cell cycle progression. The growth-inhibitory effects of TReP-132 was further shown to be mediated by induction of G(1) cyclin-dependent kinase inhibitors p21(WAF1) (p21) and p27(KIP1) (p27) expression levels. As a consequence, G(1) cyclin/cyclin-dependent kinase activities and pRB phosphorylation were markedly reduced, and cell cycle progression was blocked in the G(1) phase. The stimulatory effect of TReP-132 on p21 and p27 gene transcription involved interaction of TReP-132 with the transcription factor Sp1 at proximal Sp1-binding sites in their promoters. Moreover, in different breast tumor cell lines, endogenous TReP-132 expression was positively related with a lower proliferation rate. In addition, TReP-132 knockdown resulted in enhanced cell proliferation and lowered p21 and p27 mRNA levels in the steroid-responsive and nonresponsive T-47D and MDA-MB-231 cell lines, respectively. Finally, a statistic profiling of human breast tumor samples highlighted that expression of TReP-132 is correlated with p21 and p27 levels and is associated with lower tumor incidence and aggressiveness. Together, these results identify TReP-132 as a basal cell cycle regulatory protein acting, at least in part, by interacting with Sp1 to activate the p21 and p27 gene promoters.
Mol Cell Biol 2005 Jun
PMID:TReP-132 controls cell proliferation by regulating the expression of the cyclin-dependent kinase inhibitors p21WAF1/Cip1 and p27Kip1. 1589 40

The prognostic significance of selected markers of leukemic cells is well known. CD7 and CD56 expression at diagnosis has been associated with low remission rates and biological aggressiveness in a significant proportion of acute leukemias. Among 46 patients with acute myeloid leukemia, we found CD7 expression in 15 cases (32.6%) and CD56 positivity in 10 patients (21.7%). Six of these myeloid leukemia cases (13%) showed expression of both CD7 and CD56. Four of 46 (8.7%) patients expressed CD79a. Among the 10 that were acute myeloblastic leukemia, 8 expressed CD7, 4 expressed CD56, and 4 were positive for CD79a. Thus, these markers were expressed early in hemopoietic ontogeny in the lesser-differentiated acute myeloid leukemia subtypes, including FAB M0, M1, and M2. Whereas CD7 and CD56 were each positive in 4 cases of acute myelomonocytic leukemia (FAB M4 subtype), there was no CD79a expression in the M4 cases. CD7 is expressed by mature T cells, NK cells, and an immature myeloid cell subset. NK cells and a T cell subset express CD56. By contrast, CD79a is a B cell marker that is assigned a high score of 2.0 in the differentiation of acute leukemias of ambiguous lineage in the WHO classification. The aberrant expression of CD7, CD56, and CD79a, representing the capacity of these leukemias for trilineal expression of leukocyte differentiation antigens, portends a poor prognosis.
Exp Mol Pathol 2005 Aug
PMID:Aberrant expression of CD7, CD56, and CD79a antigens in acute myeloid leukemias. 1600 10

This study shows that high keratin 18 (K18) expression in tumor cells is associated with reduced invasiveness in vitro and lack of tumorigenicity in nude mice. We previously showed that high K18 expression correlated with a good prognosis and that reducing K18 expression increased the aggressiveness of established breast cancer cell lines. To confirm these observations, we transfected the human K18 gene into the human breast cancer cell line MDA-MB-231 and isolated a stable overexpressing clone. The forced K18 expression was associated with a complete loss of the previously strong vimentin expression in the parent cell line, induction of the K18 dimerization partner K8, and up-regulation of adhesion proteins. These changes were accompanied by a dramatic reduction in the aggressiveness of the K18 transfectants in vitro and in vivo. We conclude that forced reexpression of K18 causes at least partial redifferentiation of the tumor cell, followed by a corresponding regression of malignant phenotype.
Mol Cancer Res 2005 Jul
PMID:Transfection of keratin 18 gene in human breast cancer cells causes induction of adhesion proteins and dramatic regression of malignancy in vitro and in vivo. 1604 47

Xanthomonas campestris pv. armoraciae strain 5 is a Brassicaceae pathogen that expresses three members of the highly related avrBs3 gene family of type III effectors. Here, we report on the isolation and characterization of these genes, designated hax2, hax3, and hax4 (homolog of avrBs3 in Xanthomonas). All three Hax proteins are translocated from Xanthomonas spp. into the plant cell via the type III secretion system. Hax3 and Hax4 show the typical structure of AvrBs3-like effectors and contain a repetitive region in their central part consisting of 34-amino-acid (aa) repeats. By contrast, the Hax2 repeat region is composed of 35-aa repeats that are characterized by an additional proline residue. Hax2, Hax3, and Hax4 contain 21.5, 11.5, and 14.5 repeats, respectively. Genetic studies revealed an additive effect of hax2, hax3, and hax4 on disease symptom formation of X. campestris pv. armoraciae strain 5 on radish. The contribution of individual genes to the aggressiveness of strain 5 is quantitatively different, with hax2 showing the strongest effect on the development of chlorosis and necrosis. In addition, hax3 and hax4, but not hax2, have a Bs4-dependent avirulence activity in tomato and in transgenic Nicotiana benthamiana expressing the Bs4 resistance gene.
Mol Plant Microbe Interact 2005 Aug
PMID:Characterization of AvrBs3-like effectors from a Brassicaceae pathogen reveals virulence and avirulence activities and a protein with a novel repeat architecture. 1613 96

c-Yes is a member of the c-Src family of tyrosine kinases and has been implicated in intracellular signaling, cell morphology, and adhesion. Changes in its expression have also been associated with the aggressiveness of human breast and colon cancer cells. In MDA-MB-231 human breast cancer cells, overexpression of the small heat shock protein 27 (hsp27) results in a downregulation of c-Yes levels, concomitant with increased in vitro invasiveness and in vivo metastatic behavior. Very little is known, however, about the mechanisms regulating c-Yes expression. Here, we demonstrate that hsp27-induced c-Yes downregulation is not due to a reduction in transcriptional activity. However, the 3'-untranslated region (3'-UTR) of the c-Yes gene may be involved in its own regulation, since this region affects heterologous reporter gene activity in transactivation assays. This down-regulatory effect maps to three adenine/uridine-rich elements (AREs) that bind to cellular HuR and AUF1 (hnRNP D), two ARE-binding proteins (ARE-BPs) implicated in accelerated mRNA degradation. Our results suggest that the c-Yes 3'-UTR contains at least three newly identified AREs which are bound specifically by ARE-BPs, and provide a structural basis for post-transcriptional regulation of c-Yes expression.
J Steroid Biochem Mol Biol 2005 Nov
PMID:The c-Yes 3'-UTR contains adenine/uridine-rich elements that bind AUF1 and HuR involved in mRNA decay in breast cancer cells. 1628 64

Signaling by the insulin-like growth factor (IGF)-1 receptor (IGF-1R) has been implicated in the promotion and aggressiveness of breast, prostate, colorectal, and lung cancers. The IGF binding proteins (IGFBPs) represent a class of natural IGF antagonists that bind to and sequester IGF-1/2 from the IGF-1R, making them attractive candidates as therapeutics for cancer prevention and control. Recombinant human IGFBP-2 significantly attenuated IGF-1-stimulated MCF-7 cell proliferation with coaddition of 20 or 100 nM IGFBP-2 (50 or 80% inhibition, respectively). We previously identified IGF-1 contact sites both upstream and downstream of the CWCV motif (residues 247-250) in human IGFBP-2 (J Biol Chem 276:2880-2889, 2001). To further test their contributions to IGFBP-2 function, the single tryptophan in human IGFBP-2, Trp-248, was selectively cleaved with 2-(2'nitrophenylsulfenyl)-3-methyl-3 bromoindolenine (BNPS-skatole) and the BNPS-skatole products IGFBP-2(1-248) and IGFBP-2(249-289) as well as IGFBP-2(1-190) were expressed as glutathione S-transferase-fusion proteins and purified. Based on competition binding analysis, deletion of residues 249 to 289 caused an approximately 20-fold decrease in IGF-1 binding affinity (IGFBP-2 EC50 = 0.35 nM and IGFBP-2(1-248) = 7 nM). Removal of the remainder of the C-terminal domain had no further effect on affinity (IGFBP-2(1-190) EC50 = 9.2 nM). In kinetic assays, IGFBP-2(1-248) and IGFBP-2(1-190) exhibited more rapid association and dissociation rates than full-length IGFBP-2. These results confirm that regions upstream and downstream of the CWCV motif participate in IGF-1 binding. They further support the development of full-length IGFBP-2 as a cancer therapeutic.
Mol Pharmacol 2006 Mar
PMID:Insulin-like growth factor binding protein-2: contributions of the C-terminal domain to insulin-like growth factor-1 binding. 1630 30

Rapid, non-genomic, steroid actions have been identified for more than 20 years. In the last decade however, a great expansion of research was observed. In the present review we report the identification and the subsequent signaling cascades involved in these rapid steroid effects. In the current state of knowledge, with the exception of progesterone for which a seven-loop G protein-coupled receptor has been identified, two major lines of evidence exist for membrane-related steroid actions: (1) a binding to the intracellular receptor, coupled to the plasma membrane, or interacting with other growth factor receptors, and (2) the existence of specific membrane steroid receptors. In addition, major intracellular signaling cascades involved in cell survival and/or apoptosis are activated by non-genomic steroid actions. Finally, it appears that cancer cells and tumors express membrane steroid sites, related to cancer aggressiveness. These lines of evidence may implicate, in the forthcoming years, membrane steroid receptors in cancer control as major or adjuvant chemotherapeutic agents, providing new possible targets for cancer chemotherapy.
Mol Cell Endocrinol 2006 Feb 26
PMID:Membrane steroid receptor signaling in normal and neoplastic cells. 1642 Sep 72


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