Signal transduction最新文献_第8页

Chemical intervention in signalling networks: recent advances and applications† 信号网络中的化学干预:最新进展和应用†

Signal transduction Pub Date : 2006-04-01 DOI: 10.1002/SITA.200500075

E. Tate

{"title":"Chemical intervention in signalling networks: recent advances and applications†","authors":"E. Tate","doi":"10.1002/SITA.200500075","DOIUrl":"https://doi.org/10.1002/SITA.200500075","url":null,"abstract":"Chemical intervention in biological systems is a field undergoing explosive growth, and a growing number of applications in signal transduction have evolved from the rich variety of small molecule and other chemical tools now available for selective modulation of cellular processes. The key enabling factor for the majority of recent discoveries has been close collaboration between chemists and cell biologists, bringing together expertise in the development and application of novel and biologically-relevant chemistry and an understanding of where these techniques can be brought to bear for greatest effect. The core technologies of chemical genetics, diversity oriented synthesis, high-throughput screening and microarray technologies have recently been used in various combinations to shed light on an impressive diversity of areas, including neural lipid and auxin signalling, membrane protein co-localisation, protein kinase engineering, and imaging signalling-related processes. While further innovation is required to demonstrate the full potential for selective chemical intervention to complement and to a degree supersede pure genetic approaches, it will continue to stimulate ground-breaking research, in both chemistry and biology, for many years to come.","PeriodicalId":88702,"journal":{"name":"Signal transduction","volume":"56 1","pages":"144-159"},"PeriodicalIF":0.0,"publicationDate":"2006-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1002/SITA.200500075","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"50950459","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 8

The tumor suppressor p53 is not required for antigen receptor‐mediated apoptosis of B lymphocytes 肿瘤抑制因子p53不是抗原受体介导的B淋巴细胞凋亡所必需的

Signal transduction Pub Date : 2006-02-01 DOI: 10.1002/SITA.200400033

S. Devi, H. Hagiyama, T. Adachi, N. Miyasaka, T. Tsubata

引用次数: 0

B lymphocyte‐induced maturation protein‐1 (Blimp‐1) is sufficient to trigger an unfolded protein response and XBP‐1 processing in B cells B淋巴细胞诱导的成熟蛋白- 1 (Blimp - 1)足以触发B细胞中的未折叠蛋白反应和XBP - 1加工

Signal transduction Pub Date : 2006-02-01 DOI: 10.1002/SITA.200500048

D. Vallabhapurapu, A. Schimpl, I. Berberich

{"title":"B lymphocyte‐induced maturation protein‐1 (Blimp‐1) is sufficient to trigger an unfolded protein response and XBP‐1 processing in B cells","authors":"D. Vallabhapurapu, A. Schimpl, I. Berberich","doi":"10.1002/SITA.200500048","DOIUrl":"https://doi.org/10.1002/SITA.200500048","url":null,"abstract":"Terminal differentiation of B cells into antibody secreting plasma cells is an essential step for eliciting a successful humoral immune response. The two transcription factors B lymphocyte-induced maturation protein-1 (Blimp-1) and X-box-binding protein-1 (XBP-1) are indispensable for this process. Hereby, XBP-1 activation depends on Blimp-1. However, it is not known if Blimp-1 alone, in the absence of differentiation signals, can induce XBP-1 processing. Here we show that ectopic expression of Blimp-1 is sufficient to induce an unfolded protein response (UPR), as evidenced by the generation of the processed form of XBP-1 and upregulation of the classical UPR target BIP, in both the B cell lymphoma cell line WEHI 231 and in mouse primary splenic B cells. Interestingly, the amino terminal part of Blimp-1 comprising amino acids 1-751 was sufficient to induce the above effects while the carboxy terminal part comprising amino acids 465-856 had no effect. Taken together our results identify Blimp-1 as the upstream molecule, capable of triggering the UPR in B cells resulting in XBP-1 processing, which is an important step during plasma cell generation.","PeriodicalId":88702,"journal":{"name":"Signal transduction","volume":"29 2","pages":"62-68"},"PeriodicalIF":0.0,"publicationDate":"2006-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1002/SITA.200500048","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"50950279","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 3

Hormone receptors, MAPKs and transcription factors 激素受体，mapk和转录因子

Signal transduction Pub Date : 2006-02-01 DOI: 10.1002/SITA.200690001

R. Hass

引用次数: 1

Mitogen activated protein kinase signaling in the kidney: Target for intervention? 肾有丝分裂原激活的蛋白激酶信号:干预的目标?

Signal transduction Pub Date : 2006-02-01 DOI: 10.1002/SITA.200500063

M. D. de Borst, L. Wassef, D. Kelly, H. van Goor, G. Navis

{"title":"Mitogen activated protein kinase signaling in the kidney: Target for intervention?","authors":"M. D. de Borst, L. Wassef, D. Kelly, H. van Goor, G. Navis","doi":"10.1002/SITA.200500063","DOIUrl":"https://doi.org/10.1002/SITA.200500063","url":null,"abstract":"Mitogen activated protein kinases (MAPKs) are intracellular signal transduction molecules, which connect cell-surface receptor signals to intracellular processes. MAPKs regulate a range of cellular activities including cell proliferation, gene expression, apoptosis, cell differentiation and cytokine production. The MAPK superfamily consists of at least four families: extracellular signal-regulated kinase (ERK), p38 MAPK, Jun-NH2-terminal kinase (JNK), and ERK5. Each of these families exerts particular downstream effects, although interactions have been described. MAPK activity is present in the normal kidney. Moreover, in various types of renal disease, renal MAPK expression is increased. Interventions that provide renoprotection, such as ACE-inhibition or statin therapy, may reduce renal MAPK expression, suggesting that increased renal MAPK expression is involved in the pathophysiology of renal damage. Studies using specific MAPK inhibitors have been used to further elucidate this role. This review gives an overview of available in vitro data on MAPK activation (focussed on renal cell types), and describes MAPK localization and possible functions in the normal and diseased kidney in man, and in experimental renal disease. Studies reporting the effect of conventional renoprotective intervention on renal MAPK expression are reviewed, as well as the available data on specific MAPK inhibition, both in the clinical and experimental setting. The available data appear to support the potential of MAPK inhibition as a novel intervention strategy in renal disease, but future clinical studies are needed to substantiate this assumption, and to establish its safety. (copyright) 2006 Wiley-VCH Verlag GmbH & Co. KGaA","PeriodicalId":88702,"journal":{"name":"Signal transduction","volume":"43 2","pages":"32-53"},"PeriodicalIF":0.0,"publicationDate":"2006-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1002/SITA.200500063","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"50950512","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 20

Dissociation between M1-facilitation of acetylcholine release and crosstalk with A2A- and M2-receptors on rat motoneurons 大鼠运动神经元上乙酰胆碱释放的m1促进与A2A-和m2受体串扰的解离

Signal transduction Pub Date : 2006-02-01 DOI: 10.1002/SITA.200500057

Laura Oliveira, P. Correia-de-Sá

{"title":"Dissociation between M1-facilitation of acetylcholine release and crosstalk with A2A- and M2-receptors on rat motoneurons","authors":"Laura Oliveira, P. Correia-de-Sá","doi":"10.1002/SITA.200500057","DOIUrl":"https://doi.org/10.1002/SITA.200500057","url":null,"abstract":"Acetylcholine (ACh) facilitates its own release acting at muscarinic M1 receptors on rat motoneurons. While the M1 positive feedback mechanism is operative there is a concomitant suppression of the ability of muscarinic M2-inhibitory and adenosine A2A-facilitatory receptors to control [3H]ACh release. We aimed at investigating whether M1-occlusion of M2 and A2A receptors function could result from interplay at second messengers level. Drugs blocking the IP3 pathway, like LiCl and 2-aminoethoxydiphenylborane (2-APB), but not the selective PKC inhibitor, chelerythrine, attenuated M1 facilitation by McN-A-343. PKC activation with phorbol 12-myristate 13-acetate mimicked the ability of McN-A-343 to suppress M2-inhibition and A2A-facilitation of [3H]ACh release caused by oxotremorine and CGS 21680C, respectively. Co-application of chelerythrine together with McN-A-343 restored oxotremorine-inhibition and CGS 21680C-facilitation, but this was not observed when the M1 agonist was applied together with LiCl and 2-APB. McN-A-343 also masked facilitation of [3H]ACh release caused by stimulators of the cyclic AMP pathway, forskolin and rolipram. Data suggest that M1-facilitation of ACh release results mainly from activation of the IP3 pathway. This mechanism can be dissociated from the way M1 receptor operates suppression of neuromodulation through M2-inhibitory and A2A-facilitatory receptors, which might involve secondary PKC activation.","PeriodicalId":88702,"journal":{"name":"Signal transduction","volume":"25 3","pages":"19-31"},"PeriodicalIF":0.0,"publicationDate":"2006-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1002/SITA.200500057","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"50950322","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 5

Hypothesized and found mechanisms for potentiation of bradykinin actions. 假设并发现缓激肽作用的增效机制。

Signal transduction Pub Date : 2006-02-01 Epub Date: 2006-01-17 DOI: 10.1002/sita.200500061

Sylvia Mueller, Inge Paegelow, Siegmund Reissmann

{"title":"Hypothesized and found mechanisms for potentiation of bradykinin actions.","authors":"Sylvia Mueller, Inge Paegelow, Siegmund Reissmann","doi":"10.1002/sita.200500061","DOIUrl":"10.1002/sita.200500061","url":null,"abstract":"<p><p>Potentiation of hormone actions can occur by different mechanisms, including inhibition of degrading enzymes, interaction with the hormone receptor leading to stabilization of bioactive conformation or leading to receptor homo- and hetero-oligomerization, receptor phosphorylation and dephosphorylation or can occur by directly influencing the signal transduction and ion channels. In this review the potentiation of bradykinin actions in different systems by certain compounds will be reviewed. Despite many long years of experimental research and investigation the mechanisms of potentiating action remain not fully understood. One of the most contradictory findings are the distinct differences between the inhibition of the angiotensin I-converting enzyme and the potentiation of the bradykinin induced smooth muscle reaction. Contradictory findings and hypothesized mechanisms in the literature are discussed in this review and in some cases compared to own results. Investigation of potentiating actions was extended from hypotension, smooth muscle reaction and cellular actions to activation of immunocompetent cells. In our opinion the potentiation of bradykinin action can occur by different mechanisms, depending on the system and the applied potentiating factor used.</p>","PeriodicalId":88702,"journal":{"name":"Signal transduction","volume":"6 1","pages":"5-18"},"PeriodicalIF":0.0,"publicationDate":"2006-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7169587/pdf/SITA-6-5.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37866618","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Maillard reaction product‐rich food impair cell proliferation and induce cell death in vitro 富含美拉德反应产物的食物可抑制细胞增殖并诱导细胞死亡

Signal transduction Pub Date : 2005-12-01 DOI: 10.1002/SITA.200500066

B. Bartling, Grit Rehbein, V. Somoza, R. Silber, A. Simm

{"title":"Maillard reaction product‐rich food impair cell proliferation and induce cell death in vitro","authors":"B. Bartling, Grit Rehbein, V. Somoza, R. Silber, A. Simm","doi":"10.1002/SITA.200500066","DOIUrl":"https://doi.org/10.1002/SITA.200500066","url":null,"abstract":"Maillard reaction products (MRPs) and advanced glycation end-products (AGEs) correspond to modified protein derivatives that are initially generated by non-enzymatic glycation between amino acids and reducing sugars in heat-treated foods and in vivo, respectively. Because lung tissue highly expresses the receptor for advanced glycation end-products (RAGE), we studied the impact of MRP/AGE-rich foods like bread crust (BC) and coffee extract (CE) on the proliferation and cell death induction using lung epithelial (H358) cells. Here, we showed that CE impairs the proliferation and viability of H358 cells at much higher extent than BC does. Particularly cell death induced by CE showed a concentration-dependent shift from apoptotic to necrotic features as estimated by caspase activation, phosphatidylserine exposure, leakage of the outer membrane, mitochondrial dysfunction and stress kinase activation. Moreover, CE at higher dose triggered the generation of reactive oxygen species thereby mediating caspase inhibition. Non-toxic concentrations of both foods only impaired the proliferation associated with an increased amount of cells in the S/G2 phase of the cell cycle, which did not depend on the over-expression of RAGE. From our data we conclude that MRP/AGE-rich foods mediate antiproliferative effects at moderate concentrations that might be important in physiological conditions like cancer prevention but contributes to cell death at higher levels in vitro.","PeriodicalId":88702,"journal":{"name":"Signal transduction","volume":"6 5","pages":"303-313"},"PeriodicalIF":0.0,"publicationDate":"2005-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1002/SITA.200500066","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"50950595","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 8

Caspases and proliferation 半胱天冬酶和增殖

Signal transduction Pub Date : 2005-12-01 DOI: 10.1002/SITA.200500067

Markus Falk, M. Paulsen, S. Adam‐Klages

{"title":"Caspases and proliferation","authors":"Markus Falk, M. Paulsen, S. Adam‐Klages","doi":"10.1002/SITA.200500067","DOIUrl":"https://doi.org/10.1002/SITA.200500067","url":null,"abstract":"Cysteine-proteases belonging to the family of caspases have been described as central executioners of apoptotic signals. The relevance of apoptosis in T cell homeostasis is primarily defined by the necessity to quickly and efficiently eliminate effector T lymphocytes subsequent to clonal expansion and differentiation. This process is executed through the activation of caspases. Apoptosis can be initiated by interaction of the death receptor Fas with its ligand, triggering a signaling cascade comprising Fas-associated death domain protein (FADD), caspase-8 and caspase-3, culminating in cell death. Surprisingly, emerging evidence suggests a contribution of these molecules also in non-apoptotic and even proliferative signals. The potentially dual role of caspases does not seem to be restricted to T cells but is observed in other cells of the hematopoietic lineage as well. A block of the FADD/caspase-signaling pathway, either by inserting mutations or by using pharmacological inhibitors, not only leads to resistance of cells to apoptotic stimuli, but also negatively affects growth responses. Despite large research effort, the exact molecular mechanism how caspases mediate proliferation remains to be clarified. This review summarizes facts and hypotheses about potential junctions, coupling the opposing signals leading to death or proliferation and discusses, under which circumstances active caspases might confer to either pathway.","PeriodicalId":88702,"journal":{"name":"Signal transduction","volume":"26 2","pages":"350-355"},"PeriodicalIF":0.0,"publicationDate":"2005-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1002/SITA.200500067","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"50950642","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 1

Editorial: Apoptosis–live and let die 编辑:细胞凋亡——生与死

Signal transduction Pub Date : 2005-12-01 DOI: 10.1002/SITA.200590010

O. Janssen, R. Hass

引用次数: 1