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Other Signaling Pathways (other + signaling_pathway)
Selected AbstractsSurvival of DA neurons is independent of CREM upregulation in absence of CREBGENESIS: THE JOURNAL OF GENETICS AND DEVELOPMENT, Issue 10 2006R. Parlato Abstract cAMP response element binding protein (CREB) and the related factors CREM (cAMP response element modulator) and ATF1 (activation transcription factor 1) are bZIP-domain-containing transcription factors activated through cAMP and other signaling pathways. The disruption of CREB function in developing and mature neurons affects their development and survival when associated with loss of CREM. Since dopaminergic (DA) neurons are affected in several neurological diseases, we generated CREB conditional mutants in DA neurons by using a newly generated transgenic Cre line targeting the dopaminergic system (DATCre). Here we report the generation and analysis of mutant mice lacking CREB in DA neurons (CREBDATCre mutants). During adulthood, lack of CREB leads to a partial loss of DA neurons. Since CREM is upregulated in absence of CREB, we have introduced this mutation in a CREM,/, genetic background to assess a compensatory role of CREM. Additional inactivation of CREM does not lead to a more severe phenotype. genesis 44:454,464, 2006. © 2006 Wiley-Liss, Inc. [source] Possible Involvement of I,B Kinase 2 and MKK7 in Osteoclastogenesis Induced by Receptor Activator of Nuclear Factor ,B Ligand,JOURNAL OF BONE AND MINERAL RESEARCH, Issue 4 2002Aiichiro Yamamoto Abstract Recent studies have revealed the essential role of the receptor activator of nuclear factor ,B (NF-,B) ligand (RANKL) in osteoclast differentiation and activation. Adenovirus vector could efficiently transduce genes into RAW264.7 cells, which differentiate into osteoclast-like multinucleated cells in the presence of RANKL. The role of NF-,B and c- jun N-terminal kinase (JNK) activation in RANKL-induced osteoclast differentiation was investigated using an adenovirus vector carrying the dominant negative I,B kinase 2 gene (AxIKK2DN) or dominant negative MKK7 gene (AxMKK7DN). IKK2DN and MKK7DN overexpression in RAW cells specifically suppressed the NF-,B activation and JNK activation in response to RANKL, respectively, without affecting other signaling pathways. Either inhibition of NF-,B or JNK pathways dose-dependently inhibited osteoclast formation induced by RANKL. These results suggest that both NF-,B and JNK activation are independently required for osteoclast differentiation. [source] HIF-1 and p53: communication of transcription factors under hypoxiaJOURNAL OF CELLULAR AND MOLECULAR MEDICINE, Issue 4 2004Tobias Schmid Abstract Oxygen sensing and reactivity to changes in the concentration of oxygen is a fundamental property of cell physiology. The lack of O2 (hypoxia) is transmitted into many adaptive responses, a process that is largely controlled by a transcription factor known as hypoxia inducible factor-1 (HIF-1). More recent reports suggest that besides its traditional regulation via proteasomal degradation other signaling pathways contribute to stability regulation of the HIF-1, subunit and/or HIF-1 transactivation. These regulatory circuits allow for the integration of HIF-1 into scenarios of cell-survival vs. cell-death with the rule of the thumb that short-term mild hypoxia maintains cell viability while prolonged and severe hypoxia provokes cell demise. Cell death pathways are associated with stabilization of the tumor suppressor p53, a response also seen under hypoxic conditions. Here we summarize recent information on accumulation of HIF-1, and p53 under hypoxia and provide a model to explain the communication between HIF-1 and p53 under (patho)physiological conditions. [source] Non-conventional signal transduction by type 1 interferons: The NF-,B pathwayJOURNAL OF CELLULAR BIOCHEMISTRY, Issue 5 2007Ziyun Du Abstract Type I interferons (IFNs) regulate diverse cellular functions by modulating the expression of IFN-stimulated genes (ISGs) through the activation of the well established signal transduction pathway of the Janus Kinase (JAK) and signal transducers and activators of transcription (STAT) proteins. Although the JAK,STAT signal transduction pathway is critical in mediating IFN's antiviral and antiproliferative activities, other signaling pathways are activated by IFNs and regulate cellular response to IFN. The NF-,B transcription factor regulates the expression of genes involved in cell survival and immune responses. We have identified a novel IFN mediated signal pathway that leads to NF-,B activation and demonstrate that a subset of ISGs that play key roles in cellular response to IFN is regulated by NF-,B. This review focuses on the IFN-induced NF-,B activation pathway and the role of NF-,B in ISG expression, antiviral activity and apoptosis, and the therapeutic application of IFN in cancer and infectious disease. J. Cell. Biochem. 102: 1087,1094, 2007. © 2007 Wiley-Liss, Inc. [source] Role of TIEG1 in biological processes and disease statesJOURNAL OF CELLULAR BIOCHEMISTRY, Issue 3 2007Malayannan Subramaniam Abstract A novel TGF, Inducible Early Gene-1 (TIEG1) was discovered in human osteoblast (OB) cells by our laboratory. Over the past decade, a handful of laboratories have revealed a multitude of organismic, cellular, and molecular functions of this gene. TIEG1 is now classified as a member of the 3 zinc finger family of Krüppel-like transcription factors (KLF10). Other closely related factors [TIEG2 (KLF11) and TIEG3/TIEG2b] have been reported and are briefly compared. As described in this review, TIEG1 is shown to play a role in regulating estrogen and TGF, actions, the latter through the Smad signaling pathway. In both cases, TIEG1 acts as an inducer or repressor of gene transcription to enhance the TGF,/Smad pathway, as well at other signaling pathways, to regulate cell proliferation, differentiation, and apoptosis. This review outlines TIEG1's molecular functions and roles in skeletal disease (osteopenia/osteoporosis), heart disease (hypertrophic cardiomyopathy), and cancer (breast and prostate). J. Cell. Biochem. 102: 539,548, 2007. © 2007 Wiley-Liss, Inc. [source] TGF-, control of cell proliferationJOURNAL OF CELLULAR BIOCHEMISTRY, Issue 3 2005Shuan S. Huang Abstract This article focuses on recent findings that the type V TGF-, receptor (T,R-V), which co-expresses with other TGF-, receptors (T,R-I, T,R-II, and T,R-III) in all normal cell types studied, is involved in growth inhibition by IGFBP-3 and TGF-, and that TGF-, activity is regulated by two distinct endocytic pathways (clathrin- and caveolar/lipid-raft-mediated). TGF-, is a potent growth inhibitor for most cell types, including epithelial and endothelial cells. The signaling by which TGF-, controls cell proliferation is not well understood. Many lines of evidence indicate that other signaling pathways, in addition to the prominent T,R-I/T,R-II/Smad2/3/4 signaling cascade, are required for mediating TGF-,-induced growth inhibition. Recent studies revealed that T,R-V, which is identical to LRP-1, mediates IGF-independent growth inhibition by IGFBP-3 and mediates TGF-,-induced growth inhibition in concert with T,R-I and T,R-II. In addition, IRS proteins and a Ser/Thr-specific protein phosphatase(s) are involved in the T,R-V-mediated growth inhibitory signaling cascade. The T,R-V signaling cascade appears to cross-talk with the T,R-I/T,R-II, insulin receptor (IR), IGF-I receptor (IGF-IR), integrin and c-Met signaling cascades. Attenuation or loss of the T,R-V signaling cascade may enable carcinoma cells to escape from TGF-, growth control and may contribute to the aggressiveness and invasiveness of these cells via promoting epithelial-to-mesenchymal transdifferentiation (EMT). Finally, the ratio of TGF-, binding to T,R-II and T,R-I is a signal controlling TGF-, partitioning between two distinct endocytosis pathways and resultant TGF-, responsiveness. These recent studies have provided new insights into the molecular mechanisms underlying TGF-,-induced cellular growth inhibition, cross-talk between the T,R-V and other signaling cascades, the signal that controls TGF-, responsiveness and the role of T,R-V in tumorigenesis. © 2005 Wiley-Liss, Inc. [source] | |||||||||||||