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Same Peptide (same + peptide)
Selected AbstractsInhibition of human breast cancer cell (MBA-MD-231) invasion by the Ea4-peptide of rainbow trout pro-IGF-IJOURNAL OF CELLULAR BIOCHEMISTRY, Issue 5 2006Sineenat Siri Abstract It was shown previously that Ea4-peptide of trout pro-IGF-I exerted mitogenic activity in non-transformed cells and inhibited colony formation in a soft agar medium of established human cancer cells. Here we report that the same peptide inhibits the invasion of human breast cancer cells (MDA-MB-231) through a matrigel membrane in a dose-dependent manner. The expression of urokinase-type plasminogen activator (uPA), tissue-type plasminogen activator (tPA) and plasminogen activator inhibitor 1 (PAI1) genes in MDA-MB-231 cells were downregulated by treatment with rtEa4-peptide. The inhibition of expression of these genes in response to rtEa4-peptide treatment was reduced to the control level when inhibitors for c-Jun N-terminal kinase 1/2 (JNK1/2), mitogen activated protein kinase kinase 1/2 (Mek1/2), p38 mitogen activated protein kinase (p38 MAPK), phosphatidylinositol 3-kinase (PI3K), and phosphokinase C (PKC) were used. These results suggest that inhibition of invasion of MDA-MB-231 cells by rtEa4-peptide may be mediated via the suppression of uPA, tPA, and PAI1 gene activities through signal transduction pathways. J. Cell. Biochem. 99: 1363,1373, 2006. © 2006 Wiley-Liss, Inc. [source] Phage display identifies novel peptides that bind extracellular-regulated protein kinase 2 to compete with transcription factor binding,JOURNAL OF PHYSICAL ORGANIC CHEMISTRY, Issue 6-7 2004Mark A. Rainey Abstract Extracellular-regulated protein kinase 2 (ERK2) is a serine/threonine-specific protein kinase capable of phosphorylating multiple protein substrates within a cell. In an attempt to identify novel peptides that bind and inhibit the function of an active form of ERK2, phage display was carried out using a disulfide-constrained peptide library (X2CX14CX2). Several phage clones were identified by an enzyme-linked immunosorbent assay (ELISA) that competed with both a protein substrate and adenosine triphosphate (ATP) for immobilized ERK2. A chemically synthesized peptide derived from these experiments, NH2 -KKKIRCIRGWTKDIRTLADSCQY-COOH, inhibited ERK2 phosphorylation of the protein substrate Ets,138, exhibiting competitive and mixed inhibition towards Ets,138 and MgATP2,, respectively. Surprisingly, the same peptide displayed equally potent inhibition towards the phosphorylation of ATF2 by p38 MAPK,, another MAP kinase that has ,46% sequence similarity to ERK2. This study indicates that active ERK2 can be targeted by phage display to find novel antagonists to kinase function and suggests that protein-binding sites within the MAPK family may contain conserved features that render them susceptible to ligand binding. Copyright © 2004 John Wiley & Sons, Ltd. [source] Effects of electrospray capillary temperature on amide hydrogen exchangeRAPID COMMUNICATIONS IN MASS SPECTROMETRY, Issue 9 2008Stephen J. Coales Amide hydrogen/deuterium (H/D) exchange coupled with proteolysis, high-perfeomance liquid chromatographic (HPLC) separation and mass spectrometry (MS) has become a powerful tool to study protein dynamics in solution. Prior to the execution of H/D exchange experiments, various experimental parameters have to be set, including proteolysis, HPLC, and MS conditions. Here we investigate the effects of electrospray capillary temperature on deuterium retention in backbone amides of various pepsin-generated cytochrome c peptides. Lower capillary temperature generally helps retain more deuterium than higher capillary temperature. When the capillary temperature was 150°C, on average 26% more deuterium was retained than when the capillary temperature was set at 250°C. The effects of capillary temperature varied depending on the ions monitored. There was little difference in deuterium retention among different charge state species of the same peptide at 150°C. However, a lower charge state ion loses more deuterium atoms going from 150°C to 250°C than the corresponding higher charge state species. These results indicate that the capillary temperature should be optimized not only to maximize the signal-to-noise of each ion followed in H/D exchange experiments, but also to minimize the deuterium loss of the ions. Also the loss of deuterium in several ions, especially lower charge state ones, should be monitored in the optimization, as the temperature effects vary among ions and are more significant for lower charge state ions. Copyright © 2008 John Wiley & Sons, Ltd. [source] Autoimmune hepatitis after liver transplantation and other lessons of self-intoleranceLIVER TRANSPLANTATION, Issue 6 2002Albert J. Czaja MD Autoimmune hepatitis has been described as recurrent or de novo disease after transplantation. The legitimacy of these diagnoses and the bases for their occurrence are unknown. To better understand these aspects of allograft dysfunction, the purported pathogenic mechanisms of classical autoimmune hepatitis were reviewed and extrapolated to recurrent and de novo disease after transplantation. Loss of self-tolerance may relate to defects in the negative selection of autoreactive immunocytes and the clonal expansion of promiscuous lymphocytes that are cross-reactive to homologous antigens (molecular mimicry). Repopulation of the allograft with recipient antigen-presenting cells and the presence of primed promiscuous cytotoxic T cells within the recipient are likely factors for recurrent disease. Targets may be the same peptides that triggered the original disease, donor-derived class II antigens of the major histocompatibility complex, or homologous antigens associated with unidentified hepatotrophic viruses. De novo disease is probably due to similar mechanisms, but its predilection for children suggests that thymic dysfunction associated with cyclosporine treatment may be a factor. Corticosteroid therapy is effective in each condition. In conclusion, recurrent and de novo autoimmune hepatitis after transplantation are examples of self-intolerance. The mechanisms that perturb immunologic homeostasis in this human model of the classical disease must be studied more rigorously. [source] | ||||||||||