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At least 685 records · Page 38Linked to original sources
PubMed2005

The adapter protein GRB10 is an endogenous negative regulator of insulin-like growth factor signaling.

The growth factor IGF-I is critical for normal human somatic growth and development. Growth factor receptor-bound protein (Grb)10 is a protein that interacts with the IGF-I receptor and may thus regulate IGF-I-stimulated growth. However, the role of endogenous Grb10 in regulating IGF-I action is not known. The objective of this study was to determine the function of endogenous Grb10 in IGF signaling responses. Using small interfering RNA, we demonstrate that knockdown of Grb10 enhances IGF-I-mediated phosphorylation of insulin receptor substrate proteins, Akt/protein kinase B, and ERK1/2 and leads to a corresponding increase in DNA synthesis. Although IGF-I receptor autophosphorylation normally correlates with receptor signaling, we demonstrate a decrease in IGF-I-stimulated receptor phosphorylation in Grb10 knockdown cells. Pretreatment of cells with the protein-tyrosine phosphatase inhibitor pervanadate partially reverses this effect of Grb10 knockdown on receptor phosphorylation, indicating that endogenous Grb10 may block phosphatase access to the activated IGF-I receptor. Marked small interfering RNA knockdown of Grb10 does not result in increased or decreased expression of the related proteins Grb7 or Grb14. As further evidence for Grb10 functional specificity, the recently identified Grb10 interacting GYF proteins are shown to interact specifically with Grb10 and not with Grb7 or Grb14, using yeast two-hybrid assays. We conclude that Grb10 functions as a specific endogenous suppressor of IGF-I-stimulated cell signaling and DNA synthesis. Modulation of the Grb10-IGF-I receptor pathway may represent a mechanism that regulates IGF-I-responsive cell and tissue growth.

3T3 Cells↗
PubMed1999

An adenylyl cyclase that functions during late development of Dictyostelium.

A variety of extracellular signals lead to the accumulation of cAMP which can act as a second message within cells by activating protein kinase A (PKA). Expression of many of the essential developmental genes in Dictyostelium discoideum are known to depend on PKA activity. Cells in which the receptor-coupled adenylyl cyclase gene, acaA, is genetically inactivated grow well but are unable to develop. Surprisingly, acaA(-) mutant cells can be rescued by developing them in mixtures with wild-type cells, suggesting that another adenylyl cyclase is present in developing cells that can provide the internal cAMP necessary to activate PKA. However, the only other known adenylyl cyclase gene in Dictyostelium, acgA, is only expressed during germination of spores and plays no role in the formation of fruiting bodies. By screening morphological mutants generated by Restriction Enzyme Mediated Integration (REMI) we discovered a novel adenylyl cyclase gene, acrA, that is expressed at low levels in growing cells and at more than 25-fold higher levels during development. Growth and development up to the slug stage are unaffected in acrA(-) mutant strains but the cells make almost no viable spores and produce unnaturally long stalks. Adenylyl cyclase activity increases during aggregation, plateaus during the slug stage and then increases considerably during terminal differentiation. The increase in activity following aggregation fails to occur in acrA(-) cells. As long as ACA is fully active, ACR is not required until culmination but then plays a critical role in sporulation and construction of the stalk.

Adenylyl Cyclases↗
PubMed1999

Parental exposure, adverse pregnancy and offspring effects--perspectives in developmental epidemiology.

Developmental health is governed by biology and the societal culture that shapes family planning. This context should not be ignored in epidemiologic studies that address the effect of parental exposure from environmental and occupational agents on prenatal development, growth and survival, on adverse birth effects, or on postnatal events. It is important to have a thorough basic knowledge of developmental health in the population under study and to consider this basis in study design and performance. One way of accomplishing this task is to combine strengths of population-based cohort studies and nested case-control studies. Sibship-based cohorts and case-control studies that make use of biomarkers may provide particular advantages. Future research on the impact of parental exposure should be more strongly based on biological knowledge about the genetic, immune, and endocrine regulation of prenatal growth and development.

Environmental Exposure↗
PubMed1999

[Two individuals under the same skin--immune mechanisms in pregnancy].

The fetus may be regarded as an allograft in the maternal organism. This paper gives an overview of pregnancy-associated immune mechanisms, based on the literature and studies performed by the authors. During implantation, maternal tissues are invaded by fetal trophoblasts expressing HLA-G, a trophoblast-specific variant of HLA Class I antigens. Recognition of HLA-G stimulates uterine natural killer cells to cytokine production, by which an intrauterine immunosuppression is established. Development, growth and differentiation of placenta is regulated by the cytokines produced. Uterine leukocyte population and expression of cytokine receptors in placental tissues varies throughout gestation, and the complex interplay between trophoblasts and uterine cells, involving a number of cytokines, cytokine receptors, adhesion molecules, enzymes and hormones, changes with gestation. Some cytokines, such as tumour necrosis factor and interleukin-1, may threathen the reproductive process and fetal well-being in high doses. A tight regulation of cytokine activities is probably obtained by the observed upregulation of endogenous cytokine buffer mechanisms in pregnancy. The reproductive success and phenomenons like implantation, placental growth and development, maintenance of pregnancy and delivery, appear to rely on complex, gestational age related interplay between cells of fetal origin and the maternal immune system.

Cytokines↗
PubMedDate not supplied

Genetics of Aux/IAA and ARF action in plant growth and development.

Dramatic advances in our understanding of auxin signal-response pathways have been made in recent years. Much of this new knowledge has come through the study of mutants in Arabidopsis thaliana. Mutations have been identified in a wide variety of auxin-response components, including auxin transporters, protein kinases and phosphatases, components of a ubiquitin-proteosome pathway, and transcriptional regulators. This review focuses on mutations that affect auxin-modulated transcription factors, in particular those in the Aux/IAA and AUXIN RESPONSE FACTOR (ARF) genes. Mutants in members of these related gene families exhibit phenotypes that indicate both unique localized functions, as well as overlapping redundant functions, throughout plant development - from embryogenesis to flowering. Effects of specific mutations on Aux/IAA and ARF protein functions at the biochemical and physiological levels will be discussed. We will also discuss potential mechanisms for interactions between auxin and light response pathways that are suggested by these mutants.

Arabidopsis↗