Interaction of plexin-B1 with PDZ domain-containing Rho guanine nucleotide exchange factors

Hirotani, Mutsumi; Ohoka, Yoshiharu; Yamamoto, Takahiro; Nirasawa, Hiromi; Furuyama, Tatsuo; Kogo, Mikihiko; Matsuya, Tokuzo; Inagaki, Shinobu

doi:10.1016/s0006-291x(02)02122-8

Cited by 80 publications

(56 citation statements)

References 31 publications

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“…Similarly, Sema4D can be released from platelets by the action of metalloprotease ADAM17 (TACE), thereby acting on endothelial cells as well as platelets that also express Sema4D receptors [72]. The pro-angiogenic effect of Sema4D is mediated by the activation of a small GTPase RhoA through Rho-specific GEFs, leukemiaassociated RhoGEF, and PDZ-RhoGEF, which bind to the C-terminal PDZ-binding motif of plexin-B1 [67,[73][74][75][76]. Upon ligation of Sema4D, PDZ-RhoGEF and leukemia-associated RhoGEF are recruited to plexin-B1, thus stimulating RhoA and its downstream effector Rho kinase, and Rho kinase activation promotes angiogenic response through a chain of events involving myosin light chain phosphorylation, stress fiber contaction, nonreceptor tyrosine kinase activation, and activation of the Akt and Erk pathways [77] (Figure 3).…”

Section: Pro-angiogenic Semaphorinsmentioning

confidence: 99%

Semaphorin signaling in angiogenesis, lymphangiogenesis and cancer

2011

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Angiogenesis, the formation of new blood vessels from preexisting vasculature, is essential for many physiological processes, and aberrant angiogenesis contributes to some of the most prevalent human diseases, including cancer. Angiogenesis is controlled by delicate balance between pro-and anti-angiogenic signals. While pro-angiogenic signaling has been extensively investigated, how developmentally regulated, naturally occurring anti-angiogenic molecules prevent the excessive growth of vascular and lymphatic vessels is still poorly understood. In this review, we summarize the current knowledge on how semaphorins and their receptors, plexins and neuropilins, control normal and pathological angiogenesis, with an emphasis on semaphorin-regulated anti-angiogenic signaling circuitries in vascular and lymphatic endothelial cells. This emerging body of information may afford the opportunity to develop novel anti-angiogenic therapeutic strategies.

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Section: Pro-angiogenic Semaphorinsmentioning

confidence: 99%

Semaphorin signaling in angiogenesis, lymphangiogenesis and cancer

2011

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“…insulin-mediated glucose metabolism (24). ARHGEF11 is a member of a subfamily of RhoGEFs that contain regulator of G-protein signaling domains.…”

Section: Discussionmentioning

confidence: 99%

Variants in ARHGEF11, a Candidate Gene for the Linkage to Type 2 Diabetes on Chromosome 1q, Are Nominally Associated With Insulin Resistance and Type 2 Diabetes in Pima Indians

Hanson²,

Que³

et al. 2007

Diabetes

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A prior genome-wide linkage scan in Pima Indians indicated a young-onset (aged <45 years) type 2 diabetes susceptibility locus on chromosome 1q21-q23. ARHGEF11, which encodes the Rho guanine nucleotide exchange factor 11, was analyzed as a positional candidate gene for this linkage because this protein may stimulate Rho-dependent signals, such as the insulin signaling cascade. The ARH-GEF11 gene, and two adjacent genes NTRK1 and INSRR, were sequenced in 24 Pima Indians who were not firstdegree relatives. Sequencing of the coding regions, 5 and 3 untranslated regions and putative promoter regions of these genes, identified 28 variants in ARHGEF11, 11 variants in NTRK1, and 8 variants in INSSR. These 47 variants, as well as 84 additional public database variants within/ between these genes, were genotyped for association analysis in the same group of Pima Indians who had participated in the linkage study (n ‫؍‬ 1,228). An R1467H in ARHGEF11, and several additional noncoding variants that were in high linkage disequilibrium with this variant, were nominally associated with young-onset type 2 diabetes (P ‫؍‬ 0.01; odds ratio 3.39) after adjusting for sex, family membership, and Pima heritage. The risk allele H had a frequency of 0.10. In a subgroup of 262 nondiabetic, full-heritage Pima Indians who had undergone detailed metabolic testing, the risk allele H also was associated with a lower mean insulin-mediated glucose disposal rate and a lower mean nonoxidative glucose storage rate after adjusting for age, sex, nuclear family membership, and percentage of body fat (P < 0.01). These findings suggest that variation within ARHGEF11 nominally increases risk of type 2 diabetes, possibly as a result of increased insulin resistance.

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“…[103][104][105][106][107] This interaction is not influenced by the ligand, but depends on the association of Rnd1 to the plexin 87 and on the activity of ErbB2 tyrosine kinase recruited in the complex. 108 Therefore, in certain instances, the activation of plexins B can induce RhoA activation, which is likely to be involved in specific functional responses mediated by plexins of the B subfamily, such as the pro-angiogenic activity of Semaphorin 4D.…”

Section: Integrins and The Actin Cytoskeleton Are Major Targets Of Plmentioning

confidence: 99%

Semaphorin Signals in Cell Adhesion and Cell Migration: Functional Role and Molecular Mechanisms

Casazza¹,

Fazzari²,

Tamagnone

2007

Advances in Experimental Medicine and Biology

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C ell migration is pivotal in embryo development and in the adult. During development, a wide range of progenitor cells travel over long distances before undergoing terminal differentiation. Moreover, the morphogenesis of epithelial tissues and of the cardio-vascular system involves remodelling compact cell layers and the sprouting of new tubular branches. In the adult, cell migration is essential for the leucocytes involved in immune response. Furthermore, invasive and metastatic cancer cells have the distinctive ability to overcome normal tissue boundaries, travel in and out the blood vessels, and settle down in heterologous tissues. Cell migration normally follows strict guidance cues, either attractive, or inhibitory and repulsive. Semaphorins are a wide family of signals guiding cell migration during development and in the adult. Recent findings have established that semaphorin receptors, the plexins, govern cell migration by regulating integrin-based cell substrate adhesion and actin cytoskeleton dynamics, via specific monomeric GTPases. Plexins furthermore recruit tyrosine kinases in receptor complexes, which allows switching between multiple signalling pathways and functional outcomes. In this article, we will review the functional role of semaphorins in cell migration and the implicated molecular mechanisms controlling cell adhesion.

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Interaction of plexin-B1 with PDZ domain-containing Rho guanine nucleotide exchange factors

Cited by 80 publications

References 31 publications

Semaphorin signaling in angiogenesis, lymphangiogenesis and cancer

Semaphorin signaling in angiogenesis, lymphangiogenesis and cancer

Variants in ARHGEF11, a Candidate Gene for the Linkage to Type 2 Diabetes on Chromosome 1q, Are Nominally Associated With Insulin Resistance and Type 2 Diabetes in Pima Indians

Semaphorin Signals in Cell Adhesion and Cell Migration: Functional Role and Molecular Mechanisms

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