Cell regulation最新文献

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Transforming growth factor alpha induces collagen degradation and cell migration in differentiating human epidermal raft cultures. 转化生长因子α诱导人表皮筏培养中胶原降解和细胞迁移。
Cell regulation Pub Date : 1991-08-01 DOI: 10.1091/mbc.2.8.613
K Turksen, Y Choi, E Fuchs
{"title":"Transforming growth factor alpha induces collagen degradation and cell migration in differentiating human epidermal raft cultures.","authors":"K Turksen,&nbsp;Y Choi,&nbsp;E Fuchs","doi":"10.1091/mbc.2.8.613","DOIUrl":"https://doi.org/10.1091/mbc.2.8.613","url":null,"abstract":"<p><p>When cultured on plastic and treated with transforming growth factor alpha (TGF alpha), human keratinocytes exhibit an increase in proliferation at the colony periphery, apparently as a consequence of enhanced cell migration (Barrandon and Green, 1987). To investigate the effects of TGF alpha on a differentiating stratified squamous epithelium and to begin to examine the molecular basis mediating this influence, we cultured human epidermal cells on a gelled lattice of collagen and fibroblasts, floating on the air-liquid interface. Under these conditions, raft cultures differentiate and exhibit morphological and biochemical features of human skin in vivo (Asselineau et al., 1986; Kopan et al., 1987). When 3-wk-old raft cultures were treated with TGF alpha, basal cells showed a marked increase in cell proliferation. At elevated concentrations of TGF alpha, the organization of cells within the artificial tissue changed and islands of basal cells entered the collagen matrix. Biochemical analysis of the response revealed that type I collagenase and gelatinase were induced by keratinocytes within 12 h after TGF alpha treatment. In contrast, invasion of basal cells into the collagen matrix was not significant until 48-72 h post-treatment, suggesting that collagenase and gelatinase production may be a prerequisite to this phenomenon. These results have important implications for the possible role of TGF alpha in squamous cell carcinoma and tumor invasion.</p>","PeriodicalId":9671,"journal":{"name":"Cell regulation","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1991-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1091/mbc.2.8.613","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"12828900","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: 44
Carboxy-terminal truncations of epidermal growth factor (EGF) receptor affect diverse EGF-induced cellular responses. 表皮生长因子(EGF)受体羧基末端截断影响多种表皮生长因子诱导的细胞反应。
Cell regulation Pub Date : 1991-08-01 DOI: 10.1091/mbc.2.8.641
W Li, N Hack, B Margolis, A Ullrich, K Skorecki, J Schlessinger
{"title":"Carboxy-terminal truncations of epidermal growth factor (EGF) receptor affect diverse EGF-induced cellular responses.","authors":"W Li,&nbsp;N Hack,&nbsp;B Margolis,&nbsp;A Ullrich,&nbsp;K Skorecki,&nbsp;J Schlessinger","doi":"10.1091/mbc.2.8.641","DOIUrl":"https://doi.org/10.1091/mbc.2.8.641","url":null,"abstract":"<p><p>The binding of epidermal growth factor (EGF) to its receptor induces tyrosine phosphorylation of phospholipase C gamma (PLC gamma), which appears to be necessary for its activation leading to phosphatidyl inositol (PI) hydrolysis. Moreover, EGF-receptor (EGF-R) activation and autophosphorylation results in binding of PLC gamma to the tyrosine phosphorylated carboxy-terminus of the receptor. To gain further insights into the mechanisms and interactions regulating these processes, we have analyzed transfected NIH-3T3 cells expressing two EGF-R carboxy-terminal deletion mutants (CD63 and CD126) with reduced capacity to stimulate PI hydrolysis, Ca2+ rises, and DNA synthesis. In fact, the CD126 mutant lacking 126 carboxy-terminal amino acids, including four tyrosine autophosphorylation sites, was unable to stimulate PI hydrolysis or Ca2+ rise in response to EGF. Surprisingly, EGF binding to the cell lines expressing CD63 or CD126 mutants was followed by similar stimulation of tyrosine phosphorylation of PLC gamma. Our results suggest that although necessary, tyrosine phosphorylation of PLC gamma may not be sufficient for stimulation and PI hydrolysis. It is clear, however, that the carboxy-terminal region of EGF-R is involved in regulation of interactions with cellular targets and therefore plays a crucial role in postreceptor signaling pathways.</p>","PeriodicalId":9671,"journal":{"name":"Cell regulation","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1991-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1091/mbc.2.8.641","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"12941206","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: 16
p42/mitogen-activated protein kinase as a converging target for different growth factor signaling pathways: use of pertussis toxin as a discrimination factor. P42 /丝裂原活化蛋白激酶作为不同生长因子信号通路的会聚靶点:百日咳毒素作为鉴别因子的应用
Cell regulation Pub Date : 1991-08-01 DOI: 10.1091/mbc.2.8.675
G L'Allemain, J Pouyssegur, M J Weber
{"title":"p42/mitogen-activated protein kinase as a converging target for different growth factor signaling pathways: use of pertussis toxin as a discrimination factor.","authors":"G L'Allemain,&nbsp;J Pouyssegur,&nbsp;M J Weber","doi":"10.1091/mbc.2.8.675","DOIUrl":"https://doi.org/10.1091/mbc.2.8.675","url":null,"abstract":"<p><p>Mitogen-activated protein (MAP) kinase is a 42-kDa serine/threonine-specific protein kinase that requires phosphorylation on both tyrosine and threonine residues for activity. This enzyme is rapidly and transiently activated in quiescent cells after addition of various agonists, including insulin, epidermal growth factor, platelet-derived growth factor, and phorbol esters. We show here that addition of the growth factors thrombin or basic fibroblast growth factor to CCL39 fibroblasts rapidly induces tyrosine phosphorylation of the p42 MAP kinase protein and concomitantly stimulates MAP kinase enzymatic activity. To elucidate the signaling pathways utilized in this activation, we took advantage of the sensitivity of CCL39 cells to the toxin of bordetella pertussis, which ADP-ribosylates two Gi proteins in this cell system. We show that pretreatment of cells with the toxin inhibited thrombin stimulation of MAP kinase by greater than 75% but had no detectable effect on the stimulation induced by basic fibroblast growth factor. We also demonstrate that these two growth factors that synergize for mitogenicity are able to cooperate in activation of MAP kinase and that this synergism is partially sensitive to pertussis toxin. Finally, we describe a 44-kDa protein, the tyrosine phosphorylation of which appears to be coregulated with p42 MAP kinase. We conclude that p42 MAP kinase (and the pp44 protein) are at or are downstream from a point of convergence of two different receptor-induced signaling pathways and might well play a key role in integrating those signals.</p>","PeriodicalId":9671,"journal":{"name":"Cell regulation","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1991-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1091/mbc.2.8.675","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"12941207","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: 87
Protein phosphatases and DNA tumor viruses: transformation through the back door? 蛋白磷酸酶和DNA肿瘤病毒:通过后门转化?
Cell regulation Pub Date : 1991-08-01 DOI: 10.1091/mbc.2.8.589
M C Mumby, G Walter
{"title":"Protein phosphatases and DNA tumor viruses: transformation through the back door?","authors":"M C Mumby,&nbsp;G Walter","doi":"10.1091/mbc.2.8.589","DOIUrl":"https://doi.org/10.1091/mbc.2.8.589","url":null,"abstract":"<p><p>Cellular transformation by many oncogenic viruses is mediated by alterations in signal transduction pathways that control normal growth and proliferation. Common targets for many transforming viruses are pathways regulated by protein phosphorylation. The biochemical control of proteins in these pathways is a dynamic process that is regulated by the relative activities of protein kinases and phosphatases. Although there are numerous examples of viral oncogenes that encode protein kinases (Hunter, 1991), until recently there has been no evidence linking altered phosphatase activity to transformation. In this review we describe a novel mechanism, utilized by small DNA tumor viruses, in which viral oncogenes bind to and regulate a cellular protein serine/threonine phosphatase. The currently available evidence indicates that alteration of phosphatase activity and subsequent changes in phosphorylation levels is an important step in transformation by these viruses.</p>","PeriodicalId":9671,"journal":{"name":"Cell regulation","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1991-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1091/mbc.2.8.589","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"12828899","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: 40
Epidermal growth factor and transforming growth factor-alpha: differential intracellular routing and processing of ligand-receptor complexes. 表皮生长因子和转化生长因子:配体-受体复合物的细胞内通路和加工的差异。
Cell regulation Pub Date : 1991-08-01 DOI: 10.1091/mbc.2.8.599
R Ebner, R Derynck
{"title":"Epidermal growth factor and transforming growth factor-alpha: differential intracellular routing and processing of ligand-receptor complexes.","authors":"R Ebner,&nbsp;R Derynck","doi":"10.1091/mbc.2.8.599","DOIUrl":"https://doi.org/10.1091/mbc.2.8.599","url":null,"abstract":"<p><p>Two structurally related but different polypeptide growth factors, epidermal growth factor (EGF) and transforming growth factor-alpha (TGF-alpha), exert their activities after interaction with a common cell-surface EGF/TGF-alpha-receptor. Comparative studies of the effects of both ligands have established that TGF-alpha is more potent than EGF in a variety of biological systems. This observation is not explained by differences in affinities of the ligands for the receptor, because the affinity-constants of both factors are very similar. We have compared the intracellular processing of ligand-receptor complexes using either EGF or TGF-alpha in two different cell systems. We found that TGF-alpha dissociates from the EGF/TGF-alpha-receptor at much higher pH than EGF, which may reflect the substantial difference in the calculated isoelectric points. After internalization, the intracellular TGF-alpha is more rapidly cleared than EGF, and a substantial portion of the released TGF-alpha represents undegraded TGF-alpha in contrast to the mostly degraded EGF. In addition, TGF-alpha did not induce a complete down-regulation of cell surface receptors, as observed with EGF, which is at least in part responsible for a much sooner recovery of the ligand-binding ability after down-regulation, in the case of TGF-alpha. These differences in processing of the ligand-receptor complexes may explain why TGF-alpha exerts quantitatively higher activities than EGF.</p>","PeriodicalId":9671,"journal":{"name":"Cell regulation","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1991-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1091/mbc.2.8.599","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"12941204","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: 224
Regulatory functions of a non-ligand-binding thyroid hormone receptor isoform. 非配体结合甲状腺激素受体异构体的调节功能。
Cell regulation Pub Date : 1991-07-01 DOI: 10.1091/mbc.2.7.565
T Hermann, X K Zhang, M Tzukerman, K N Wills, G Graupner, M Pfahl
{"title":"Regulatory functions of a non-ligand-binding thyroid hormone receptor isoform.","authors":"T Hermann,&nbsp;X K Zhang,&nbsp;M Tzukerman,&nbsp;K N Wills,&nbsp;G Graupner,&nbsp;M Pfahl","doi":"10.1091/mbc.2.7.565","DOIUrl":"https://doi.org/10.1091/mbc.2.7.565","url":null,"abstract":"<p><p>Gene regulation by thyroid hormones is mediated through multiple nuclear receptors. Only some of these thyroid hormone receptor (TR) isoforms become transcriptional enhancers in the presence of the thyroid hormone T3. Here we analyze the regulatory function of the human TR alpha 2 isoform. This protein does not bind T3 and is not a transcriptional activator of thyroid hormone-responsive elements (TRE). Transfected TR alpha 2 functions as a constitutive repressor of the transcriptional activators TR alpha 1 and TR beta 1 but also represses heterologous receptors, including the retinoic acid receptor and the estrogen receptor, which can activate TRE-controlled genes. TR alpha 2 protein showed strongly reduced DNA binding to a palindromic TRE when compared with the active TRs. Hybrid receptor analysis revealed that the special properties of the TR alpha 2 protein, including its repressor function and DNA binding characteristics, are intrinsic properties of its carboxyterminus and can be transferred to other receptors. Although it has been shown that the active TRs can act as repressors and silencers due to their strong DNA binding in the absence of hormone, our data show that TR alpha 2 is unlikely to inhibit TRs and other receptors through a competitive DNA binding mechanism. Antibody gel shift experiments suggest that repression by TR alpha 2 might result from interaction with active receptors. Thus, the receptor-like TR alpha 2 isoform differs from typical nuclear receptors in its DNA-binding and ligand-binding properties and appears to regulate the activity of other receptors via protein-protein interaction.</p>","PeriodicalId":9671,"journal":{"name":"Cell regulation","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1991-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1091/mbc.2.7.565","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"12944956","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: 24
Transforming growth factor-beta (TGF-beta) isoforms in rat liver regeneration: messenger RNA expression and activation of latent TGF-beta. 转化生长因子- β (tgf - β)亚型在大鼠肝脏再生中的表达:信使RNA的表达和潜在tgf - β的激活。
Cell regulation Pub Date : 1991-07-01 DOI: 10.1091/mbc.2.7.535
S B Jakowlew, J E Mead, D Danielpour, J Wu, A B Roberts, N Fausto
{"title":"Transforming growth factor-beta (TGF-beta) isoforms in rat liver regeneration: messenger RNA expression and activation of latent TGF-beta.","authors":"S B Jakowlew,&nbsp;J E Mead,&nbsp;D Danielpour,&nbsp;J Wu,&nbsp;A B Roberts,&nbsp;N Fausto","doi":"10.1091/mbc.2.7.535","DOIUrl":"https://doi.org/10.1091/mbc.2.7.535","url":null,"abstract":"<p><p>Expression of transforming growth factor-beta s (TGF-beta s) 1-3 was studied in normal liver and during liver regeneration after partial hepatectomy in the rat to determine whether each of these isoforms might be involved in hepatocyte growth in vivo. Expression of the mRNAs for all three TGF-beta isoforms increases in the regenerating liver. In addition, the levels of expression of the mRNAs for several extracellular matrix proteins, including fibronectin, vitronectin, laminin, and collagen, also increase in the regenerating liver. Immunohistochemical staining analysis shows a similar distribution of all three TGF-beta s in normal and regenerating liver; however, in both tissues, the level of expression of TGF-beta 1 is 8- to 10-fold higher than that of TGF-beta 2 as determined by sandwich enzyme-linked immunosorbent assay. Expression of all three TGF-beta mRNAs is restricted to liver nonparenchymal cells. Although hepatocytes from normal and regenerating livers do not synthesize TGF-beta, they are sensitive to inhibition of growth by all three TGF-beta isoforms. Hepatocytes from regenerating livers are capable of activating latent TGF-beta 1 complexes in vitro, whereas normal hepatocytes are not. The different TGF-beta isoforms may function in an inhibitory paracrine mechanism that is activated during liver regeneration and may also regulate the synthesis of extracellular matrix components in the regenerating liver.</p>","PeriodicalId":9671,"journal":{"name":"Cell regulation","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1991-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1091/mbc.2.7.535","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"12944955","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: 129
p67SRF is a constitutive nuclear protein implicated in the modulation of genes required throughout the G1 period. p67SRF是一个组成核蛋白,参与G1期所需基因的调节。
Cell regulation Pub Date : 1991-07-01 DOI: 10.1091/mbc.2.7.575
C Gauthier-Rouvière, J C Cavadore, J M Blanchard, N J Lamb, A Fernandez
{"title":"p67SRF is a constitutive nuclear protein implicated in the modulation of genes required throughout the G1 period.","authors":"C Gauthier-Rouvière,&nbsp;J C Cavadore,&nbsp;J M Blanchard,&nbsp;N J Lamb,&nbsp;A Fernandez","doi":"10.1091/mbc.2.7.575","DOIUrl":"https://doi.org/10.1091/mbc.2.7.575","url":null,"abstract":"<p><p>Indirect immunofluorescence analysis, using antibodies directed against peptide sequences outside the DNA-binding domain of the 67-kDa serum response factor (p67SRF), revealed a punctuated nuclear staining, constant throughout the cell cycle and in all different cell lines tested. p67SRF was also tightly associated with chromatin through all stages of mitosis. Inhibition of p67SRF activity in vivo, through microinjection of anti-p67SRF antibodies, specifically suppressed DNA synthesis induced after serum addition or ras microinjection, suggesting that these antibodies were effective in preventing expression of serum response element (SRE)-regulated genes. A similar inhibition was also obtained in cells injected with oligonucleotides corresponding to the DNA binding sequence for p67SRF protein, SRE. Moreover, this inhibition of DNA synthesis by anti-p67SRF or SRE injection was still observed in cells injected during late G1, well after c-fos induction. These data imply that genes regulated by p67SRF are continuously involved in the proliferation pathway throughout G1 and that p67SRF forms an integral component of mammalian cell transcriptional control.</p>","PeriodicalId":9671,"journal":{"name":"Cell regulation","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1991-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1091/mbc.2.7.575","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"12944958","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: 65
Influenza virus hemagglutinin trimers and monomers maintain distinct biochemical modifications and intracellular distribution in brefeldin A-treated cells. 流感病毒血凝素三聚体和单体在brefeldin a处理的细胞中维持不同的生化修饰和细胞内分布。
Cell regulation Pub Date : 1991-07-01 DOI: 10.1091/mbc.2.7.549
G Russ, J R Bennink, T Bächi, J W Yewdell
{"title":"Influenza virus hemagglutinin trimers and monomers maintain distinct biochemical modifications and intracellular distribution in brefeldin A-treated cells.","authors":"G Russ,&nbsp;J R Bennink,&nbsp;T Bächi,&nbsp;J W Yewdell","doi":"10.1091/mbc.2.7.549","DOIUrl":"https://doi.org/10.1091/mbc.2.7.549","url":null,"abstract":"<p><p>Brefeldin A (BFA) induces the retrograde transport of proteins from the Golgi complex (GC) to the endoplasmic reticulum (ER). It is uncertain, however, whether the drug completely merges the ER with post-ER compartments, or whether some of their elements remain physically and functionally distinct. We investigated this question by the use of monoclonal antibodies specific for monomers and trimers of the influenza virus hemagglutinin (HA). In untreated influenza virus-infected cells, monomers and trimers almost exclusively partition into the ER and GC, respectively. In BFA-treated cells, both monomers and trimers are detected in the ER by immunofluorescence. Cell fractionation experiments indicate, however, that whereas HA monomers synthesized in the presence of BFA reside predominantly in vesicles with a characteristic density of the ER, HA trimers are primarily located in lighter vesicles characteristic of post-ER compartments. Biochemical experiments confirm that in BFA-treated cells, trimers are more extensively modified than monomers by GC-associated enzymes. Additional immunofluorescence experiments reveal that in BFA-treated cells, HA monomers can exist in an ER subcompartment less accessible to trimers and, conversely, that trimers are present in a vesicular compartment less accessible to monomers. These findings favor the existence of a post-ER compartment for which communication with the ER is maintained in the presence of BFA and suggest that trimers cycle between this compartment and the ER, but have access to only a portion of the ER.</p>","PeriodicalId":9671,"journal":{"name":"Cell regulation","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1991-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1091/mbc.2.7.549","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"12830168","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: 25
Identification of chicken embryo kinase 5, a developmentally regulated receptor-type tyrosine kinase of the Eph family. 鸡胚激酶5 (Eph家族发育调控受体型酪氨酸激酶)的鉴定。
Cell regulation Pub Date : 1991-07-01 DOI: 10.1091/mbc.2.7.523
E B Pasquale
{"title":"Identification of chicken embryo kinase 5, a developmentally regulated receptor-type tyrosine kinase of the Eph family.","authors":"E B Pasquale","doi":"10.1091/mbc.2.7.523","DOIUrl":"https://doi.org/10.1091/mbc.2.7.523","url":null,"abstract":"<p><p>Chicken embryo kinase 5 (Cek5) is a transmembrane tyrosine kinase of the Eph family that was identified by screening a 10-d chicken embryo cDNA expression library with anti-phosphotyrosine antibodies. The extracellular region of Cek5 contains a cysteine rich N-terminal subdomain and a C-terminal subdomain mostly devoid of cysteines and comprising two repeats similar to fibronectin type III repeats. Immunoblotting experiments with anti-Cek5 polyclonal antibodies indicated that Cek5 is a membrane-associated 120-kDa protein containing intramolecular (but not intermolecular) disulfide bonds. Cek5 is already expressed in 2-d-old chicken embryos and is also expressed, at higher levels, later in development. In 10-d-old chicken embryos, Cek5 is expressed at substantial levels in nearly all the tissues examined, whereas in adult it is expressed predominantly in the brain. The expression of Cek5 in the brain gradually diminishes during embryonic development, whereas in the skeletal muscle of the thigh a sharp decrease in Cek5 expression was detected at the time of terminal muscle differentiation. Its wide tissue distribution throughout development and its sustained expression in adult brain suggest that Cek5 is an important component of signal transduction pathways, likely to interact with a widely distributed and important ligand, which is as yet unknown.</p>","PeriodicalId":9671,"journal":{"name":"Cell regulation","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1991-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1091/mbc.2.7.523","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"12830166","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: 62
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