Relevant bibliographies by topics / Phosphoisoform

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Academic literature on the topic 'Phosphoisoform'

Author: Grafiati
Published: 10 March 2023

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Journal articles on the topic "Phosphoisoform"

1

Matsuzaki, Koichi. "Smad phosphoisoform signaling specificity: the right place at the right time." Carcinogenesis 32, no. 11 (July 27, 2011): 1578–88. http://dx.doi.org/10.1093/carcin/bgr172.

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2

Lampe, P. D., W. E. Kurata, B. J. Warn-Cramer, and A. F. Lau. "Formation of a distinct connexin43 phosphoisoform in mitotic cells is dependent upon p34cdc2 kinase." Journal of Cell Science 111, no. 6 (March 15, 1998): 833–41. http://dx.doi.org/10.1242/jcs.111.6.833.

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The gap junction protein connexin43 is a phosphoprotein that typically migrates as three bands (nonphosphorylated, P1 and P2) during polyacrylamide gel electrophoresis. The electrophoretic mobility of connexin43 from mitotic cells was distinctly reduced to a form (P3) that migrated slower than P2 from Rat1 cells prepared by shakeoff of nocodazole-treated and untreated cultures. Mitotic FT210 cells, which contain a temperature-sensitive mutation in the p34(cdc2) kinase, showed abundant levels of the P3 connexin43 when maintained at the permissive temperature where p34(cdc2) is active. In contrast, nocodozole-treated FT210 cells grown at the nonpermissive temperature did not contain P3 connexin43. These results indicated that generation of the P3 connexin43 was dependent upon active p34(cdc2)/cyclin B kinase. Although the p34(cdc2)kinase phosphorylated connexin43 in vitro on peptides containing serine 255, the major phosphotryptic peptides in P3 connexin43 from mitotic cells appeared to be the consequence of another protein kinase(s), which may be activated by the p34(cdc2)/cyclin B kinase. The P3 connexin43 exhibited a marked redistribution from cell-cell plasma membrane interfaces to multiple, distinctly stained cytoplasmic structures. These events may be part of the dramatic structural changes observed in mitotic cells undergoing cell rounding and cytokinesis. Results of initial studies using inhibitors of protein degradative and synthetic pathways suggested the likelihood that protein degradation and synthesis participate in the disappearance of the P3 connexin43 and restoration of the pattern of connexin43 isoforms observed in nonmitotic cells.
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3

Chen, Yuxin, Ziping Zhou, Qigui Mo, Gao Zhou, and Youwei Wang. "Gallic Acid Attenuates Dimethylnitrosamine-Induced Liver Fibrosis by Alteration of Smad Phosphoisoform Signaling in Rats." BioMed Research International 2018 (December 2, 2018): 1–14. http://dx.doi.org/10.1155/2018/1682743.

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Dimethylnitrosamine (DMN) is a potent hepatotoxin, carcinogen, and mutagen. In our previous study, a candidate gallic acid (GA) that widely exists in food and fruit was selected for its capability to alleviate DMN toxicity in vivo. We aimed to investigate the therapeutic potential of GA against DMN-induced liver fibrosis. During the first four weeks, DMN was administered to rats via intraperitoneal injection every other day, except the control group. GA or silymarin was given to rats by gavage once daily from the second to the sixth week. GA significantly reduced liver damage in serum parameters and improved the antioxidant capacity in liver and kidney tissues. Cytokines involved in liver fibrosis were measured at transcriptional and translational levels. These results indicate that GA exhibits robust antioxidant and antifibrosis effects and may be an effective candidate natural medicine for liver fibrosis treatment.
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Peffer, Melanie E., Janie Y. Zhang, Leah Umfrey, Anthony C. Rudine, A. Paula Monaghan, and Donald B. DeFranco. "Minireview: The Impact of Antenatal Therapeutic Synthetic Glucocorticoids on the Developing Fetal Brain." Molecular Endocrinology 29, no. 5 (May 1, 2015): 658–66. http://dx.doi.org/10.1210/me.2015-1042.

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Abstract The life-threatening, emotional, and economic burdens of premature birth have been greatly alleviated by antenatal glucocorticoid (GC) treatment. Antenatal GCs accelerate tissue development reducing respiratory distress syndrome and intraventricular hemorrhage in premature infants. However, they can also alter developmental processes in the brain and trigger adverse behavioral and metabolic outcomes later in life. This review summarizes animal model and clinical studies that examined the impact of antenatal GCs on the developing brain. In addition, we describe studies that assess glucocorticoid receptor (GR) action in neural stem/progenitor cells (NSPCs) in vivo and in vitro. We highlight recent work from our group on two GR pathways that impact NSPC proliferation, ie, a nongenomic GR pathway that regulates gap junction intercellular communication between coupled NSPCs through site-specific phosphorylation of connexin 43 and a genomic pathway driven by differential promoter recruitment of a specific GR phosphoisoform.
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Okazaki, Kazuichi. "Involvement of Smad3 phosphoisoform-mediated signaling in the development of colonic cancer in IL-10-deficient mice." International Journal of Oncology 32, no. 6 (June 1, 1992): 1221–26. http://dx.doi.org/10.3892/ijo_32_6_1221.

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6

Matsuzaki, Koichi. "Smad phosphoisoform signals in acute and chronic liver injury: similarities and differences between epithelial and mesenchymal cells." Cell and Tissue Research 347, no. 1 (May 31, 2011): 225–43. http://dx.doi.org/10.1007/s00441-011-1178-6.

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7

Mehlen, P., C. Kretz-Remy, J. Briolay, P. Fostan, M. E. Mirault, and A. P. Arrigo. "Intracellular reactive oxygen species as apparent modulators of heat-shock protein 27 (hsp27) structural organization and phosphorylation in basal and tumour necrosis factor α-treated T47D human carcinoma cells." Biochemical Journal 312, no. 2 (December 1, 1995): 367–75. http://dx.doi.org/10.1042/bj3120367.

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The small stress protein heat-shock protein 27 (hsp27) is an oligomeric phosphoprotein, constitutively expressed in most human cells, which enhances cellular resistance to tumour necrosis factor alpha (TNF alpha). This phenomenon correlates with dramatic changes in hsp27 cellular location, structural organization and phosphorylation. To gain a better understanding of the molecular mechanisms regulating these properties of hsp27, we investigated whether they were a consequence of the intracellular production of reactive oxygen species (ROS) generated by TNF alpha. Here, we report that, in T47D carcinoma cell lines, the rapid burst of intracellular ROS production and changes in hsp27 locale, structural organization and phosphoisoform composition induced by TNF alpha were abolished by the overexpression of the antioxidant enzyme seleno-glutathione peroxidase (GSHPx). These effects were greatly diminished when GSHPx-expressing cells were grown in the absence of selenium, a cofactor that is essential for seleno-GSHPx activity, indicating that they are directly linked to the increased GSHPx activity. Moreover, in growing T47D cells, GSHPx expression induced intracellular redistribution of hsp27 and decreased the phosphorylation of this protein without altering its pattern of oligomerization. In contrast, the heat-mediated phosphorylation of hsp27 was not altered by decreased intracellular ROS levels. Hence, in growing and TNF-treated cells, several hsp27 properties appear to be modulated by fluctuations in intracellular ROS levels.
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8

Magnan, Antoine, Vincenzo Di Bartolo, Anne-Marie Mura, Claude Boyer, Mireille Richelme, Yea-Lih Lin, Agnès Roure, et al. "T Cell Development and T Cell Responses in Mice with Mutations Affecting Tyrosines 292 or 315 of the Zap-70 Protein Tyrosine Kinase." Journal of Experimental Medicine 194, no. 4 (August 20, 2001): 491–506. http://dx.doi.org/10.1084/jem.194.4.491.

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After stimulation of the T cell receptor (TCR), the tyrosine residues 292 and 315 in interdomain B of the protein tyrosine kinase ZAP-70 become phosphorylated and plausibly function as docking sites for Cbl and Vav1, respectively. The two latter proteins have been suggested to serve as substrates for ZAP-70 and to fine-tune its function. To address the role of these residues in T cell development and in the function of primary T cells, we have generated mice that express ZAP-70 molecules with Tyr to Phe substitution at position 292 (Y292F) or 315 (Y315F). When analyzed in a sensitized TCR transgenic background, the ZAP-70 Y315F mutation reduced the rate of positive selection and delayed the occurrence of negative selection. Furthermore, this mutation unexpectedly affected the constitutive levels of the CD3-ζ p21 phosphoisoform. Conversely, the ZAP-70 Y292F mutation upregulated proximal events in TCR signaling and allowed more T cells to produce interleukin 2 and interferon γ in response to a given dose of antigen. The observation that ZAP-70 Y292F T cells have a slower rate of ligand-induced TCR downmodulation suggests that Y292 is likely involved in regulating the duration activated TCR reside at the cell surface. Furthermore, we showed that Y292 and Y315 are dispensable for the TCR-induced tyrosine phosphorylation of Cbl and Vav1, respectively. Therefore, other molecules present in the TCR signaling cassette act as additional adaptors for Cbl and Vav1. The present in vivo analyses extend previous data based on transformed T cell lines and suggest that residue Y292 plays a role in attenuation of TCR signaling, whereas residue Y315 enhances ZAP-70 function.
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9

Popovic, Natasa, Ana Niciforovic, Miroslav Adzic, Marija Radojcic, Constantinos Demonacos, and Marija Krstic-Demonacos. "Western blot analysis of glucocorticoid receptor phosphoisoforms by one- and two-dimensional electrophoretic assays." Journal of the Serbian Chemical Society 74, no. 3 (2009): 237–44. http://dx.doi.org/10.2298/jsc0903237p.

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The glucocorticoid receptor (GR) protein is a cytosolic ligand-dependent transcription factor with numerous functions regulated by post-translational modifications, including phosphorylation/dephosphorylation. Among the functions most extensively affected by GR phosphorylation are the modulation of its transcriptional activity, alterations in its interaction pattern with cofactors, nuclear translocation and selective gene transactivation. Intensive analysis of the intracellular distribution of GR phosphoisoforms and their interaction with proteins of other cellular signalling networks required the use of [?-32P]ATP as a phosphate donor, and special laboratory protection measures to avoid external irradiation and contamination. In the present study, simple and easy-to-use non-radioactive protein mobility shift assays (NMS assays) were developed using one- and/or two-dimensional gel electrophoresis based on differences in the pI and molecular mass of GR phosphoisoforms. The GR isoforms were immunodetected with specific monoclonal or polyclonal anti-GR antibodies by Western blot in three diverse systems, namely yeast BJ2168 cells expressing wild-type rat GR, rat hepatoma GRH2 cells grown in culture and brain tissue from Wistar rat experimental animals. The results obtained using the NMS assay were similar to previous results obtained with the [?-32P] ATP standard assay.
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10

Kim, Seok-Hyung, Kyung-Hee Kim, Soomin Ahn, Jiyeon Hyeon, and Cheol-Keun Park. "Smad3 and Smad3 Phosphoisoforms Are Prognostic Markers of Gastric Carcinoma." Digestive Diseases and Sciences 58, no. 4 (November 18, 2012): 989–97. http://dx.doi.org/10.1007/s10620-012-2470-3.

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Dissertations / Theses on the topic "Phosphoisoform"

1

NEGRI, AIDE. "Serine 10 phosphorylation in p27Kip1 metabolism: studies on wild type protein and glycine 9 arginine oncogenic mutant." Doctoral thesis, 2016. http://hdl.handle.net/2158/1036571.

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p27Kip1 is a Cyclin-dependent Kinase Inhibitor (CKI) belonging to CIP/Kip protein family. It is essentially known for its inhibitory action on several cyclin/CDK complexes (specifically cyclin E(A)/CDK2 and cyclin A(B)/CDK1), suggesting a role as tumor suppressor. However, when localized in cytosol, p27Kip1 has a number of CDK-independent functions, including the regulation of apoptosis, cell motility and differentiation. Some of these activities can enhance malignant transformation and/or metastasization under specific conditions. p27Kip1 is characterized by the lack of a stable tertiary structure that favors its “adaptability” to bind different targets and contributes to the heterogeneity of its functions. Because of this peculiar structure, the presence of several post translational modifications (especially phosphorylation) has a key relevance for the CKI cellular localization, metabolism and functions. In this study, we have investigated the turn-over and cyclins/CDK interactions of phosphoserine10-p27Kip1 (pSer10p27Kip1), the main CKI phosphoisoform. We also examined the localization, metabolism, phosphoisoforms pattern and interaction of a cancer-associated mutant form of the CKI (namely G9Rp27Kip1) in which glycine 9 is substituted by an arginine. Our attention focused on this p27Kip1 mutant since the residue change (i.e. glycine 9) occurs in the amino acid preceding serine 10 thus allowing the hypothesis that the mutation affects Ser10 post translational modification.
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