The transcription factor CREB -- for 'cyclic AMP response element-binding protein' -- functions in glucose homeostasis, growth-factor-dependent cell survival, and has been implicated in learning and memory. CREB is phosphorylated in response to various signals, but how is specificity achieved in these signalling pathways?

Transcriptional regulation by the phosphorylation-dependent factor CREB

The protein kinase B/Akt signalling pathway in human malignancy.

Recent research has examined Akt and Akt-related serine-threonine kinases in signaling cascades that regulate cell survival and are important in the pathogenesis of degenerative diseases and in cancer. We seek to recapitulate the research that has helped to define the current understanding of the role of the Akt pathway under normal and pathologic conditions, also in view of genetic models of Akt function. In particular, we will evaluate the mechanisms of Akt regulation and the role of Akt substrates in Akt-dependent biologic responses in the decisions of cell death and cell survival. Here, we hope to establish the mechanisms of apoptosis suppression by Akt kinase as a framework for a more general understanding of growth factor-dependent regulation of cell survival.

PI3K/Akt and apoptosis: size matters.

Mature tubular epithelial cells in adult kidney can undergo epithelial-to-mesenchymal transition (EMT), a phenotypic conversion that is fundamentally linked to the pathogenesis of renal interstitial fibrosis. Emerging evidence indicates that a large proportion of interstitial fibroblasts are actually originated from tubular epithelial cells via EMT in diseased kidney. Moreover, selective blockade of EMT in a mouse genetic model dramatically reduces fibrotic lesions after obstructive injury, underscoring a definite importance of EMT in renal fibrogenesis. Tubular EMT is proposed as an orchestrated, highly regulated process that consists of four key steps: (1) loss of epithelial cell adhesion; (2) de novo alpha-smooth muscle actin expression and actin reorganization; (3) disruption of tubular basement membrane; and (4) enhanced cell migration and invasion. Of the many factors that regulate EMT in different ways, transforming growth factor-beta1 is the most potent inducer that is capable of initiating and completing the entire EMT course, whereas hepatocyte growth factor and bone morphogenetic protein-7 act as EMT inhibitors both in vitro and in vivo. Multiple intracellular signaling pathways have been implicated in mediating EMT, in which Smad/integrin-linked kinase may play a central role. This article attempts to provide a comprehensive review of recent advances on understanding the pathologic significance, molecular mechanism, and therapeutic intervention of EMT in the setting of chronic renal fibrosis.

/pdf/epithelial-to-mesenchymal-transition-in-renal-fibrogenesis-pbbi42tg6l.pdf

Epithelial to Mesenchymal Transition in Renal Fibrogenesis: Pathologic Significance, Molecular Mechanism, and Therapeutic Intervention

Cyclin D1 encodes the regulatory subunit of a holoenzyme that phosphorylates and inactivates the retinoblastoma protein and promotes progression through the G1-S phase of the cell cycle. Amplification or overexpression of cyclin D1 plays pivotal roles in the development of a subset of human cancers including parathyroid adenoma, breast cancer, colon cancer, lymphoma, melanoma, and prostate cancer. Of the three D-type cyclins, each of which binds cyclin-dependent kinase (CDK), it is cyclin D1 overexpression that is predominantly associated with human tumorigenesis and cellular metastases. In recent years accumulating evidence suggests that in addition to its original description as a CDK-dependent regulator of the cell cycle, cyclin D1 also conveys cell cycle or CDK-independent functions. Cyclin D1 associates with, and regulates activity of, transcription factors, coactivators and corepressors that govern histone acetylation and chromatin remodeling proteins. The recent findings that cyclin D1 regulates cellular metabolism, fat cell differentiation and cellular migration have refocused attention on novel functions of cyclin D1 and their possible role in tumorigenesis. In this review, both the classic and novel functions of cyclin D1 are discussed with emphasis on the CDK-independent functions of cyclin D1.

Minireview: Cyclin D1: normal and abnormal functions.

The integrin-linked kinase regulates the cyclin D1 gene through glycogen synthase kinase 3beta and cAMP-responsive element-binding protein-dependent pathways.

L'invention concerne une methode d'isolation de polynucleotides codant des polypeptides qui affectent l'organisation d'un organite ou d'une structure intracellulaire recherche. Cette methode consiste a: (a) exprimer dans une pluralite de cellules une banque d'expression contenant une pluralite de produits recombines d'expression codant chacun un polypeptide recherche; (b) marquer l'organite ou la structure intracellulaire recherche contenu dans la pluralite de cellules; et enfin, (c) isoler une ou plusieurs cellules parmi la pluralite de cellules dans laquelle la distribution cellulaire et/ou le niveau de l'organite ou de la structure intracellulaire recherche est modifie, de maniere a isoler les polypeptides capables d'affecter l'organisation de l'organite ou de la structure intracellulaire recherche.

Methodes d'isolation de genes codant des proteines a fonction specifique et de criblage d'agents actifs d'un point de vue pharmaceutique

β-Catenin can play different roles in the cell, including one as a structural protein at cell-cell adherens junctions and another as a transcriptional activator mediating Wnt signal transduction. Plakoglobin (γ-catenin), a close homolog of βcatenin, shares with β-catenin common protein partners and can fulfill some of the same functions. The complexing of catenins with various protein partners is regulated by phosphorylation and by intramolecular interactions. The competition between different catenin partners for binding to catenins mediates the cross-talk between cadherin-based adhesion, catenin-dependent transcription and Wnt signaling. Although plakoglobin differs from βcatenin in its functions and is unable to compensate for defects in Wnt signaling resulting from lack of β-catenin, recent evidence suggests that plakoglobin plays a unique role in Wnt signaling that is different from that of βcatenin. The functional difference between catenins is reflected in their differential involvement in embryonic development and cancer progression. SUMMARY

COMMENTARY Plakoglobin and β-catenin: protein interactions, regulation and biological roles

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The integrin-linked kinase regulates the cyclin D1 gene through glycogen synthase kinase 3beta and cAMP-responsive element-binding protein-dependent pathways.

Methodes d'isolation de genes codant des proteines a fonction specifique et de criblage d'agents actifs d'un point de vue pharmaceutique

COMMENTARY Plakoglobin and β-catenin: protein interactions, regulation and biological roles