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Articles de revues sur le sujet « Phosphoisoform »

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Auteur : Grafiati
Publié le 10 mars 2023

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1

Matsuzaki, Koichi. « Smad phosphoisoform signaling specificity : the right place at the right time ». Carcinogenesis 32, no 11 (27 juillet 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 et A. F. Lau. « Formation of a distinct connexin43 phosphoisoform in mitotic cells is dependent upon p34cdc2 kinase ». Journal of Cell Science 111, no 6 (15 mars 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 et Youwei Wang. « Gallic Acid Attenuates Dimethylnitrosamine-Induced Liver Fibrosis by Alteration of Smad Phosphoisoform Signaling in Rats ». BioMed Research International 2018 (2 décembre 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 et Donald B. DeFranco. « Minireview : The Impact of Antenatal Therapeutic Synthetic Glucocorticoids on the Developing Fetal Brain ». Molecular Endocrinology 29, no 5 (1 mai 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 (1 juin 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 (31 mai 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 et 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 (1 décembre 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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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 (20 août 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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Popovic, Natasa, Ana Niciforovic, Miroslav Adzic, Marija Radojcic, Constantinos Demonacos et 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 et Cheol-Keun Park. « Smad3 and Smad3 Phosphoisoforms Are Prognostic Markers of Gastric Carcinoma ». Digestive Diseases and Sciences 58, no 4 (18 novembre 2012) : 989–97. http://dx.doi.org/10.1007/s10620-012-2470-3.

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11

Rocha, Mar García, et Jesús Avila. « Characterization of microtubule-associated protein phosphoisoforms present in isolated growth cones ». Developmental Brain Research 89, no 1 (octobre 1995) : 47–55. http://dx.doi.org/10.1016/0165-3806(95)00105-m.

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Hama, Taketsugu, Koichi Nakanishi, Masashi Sato, Hironobu Mukaiyama, Hiroko Togawa, Yuko Shima, Masayasu Miyajima et al. « Aberrant Smad3 phosphoisoforms in cyst-lining epithelial cells in the cpk mouse, a model of autosomal recessive polycystic kidney disease ». American Journal of Physiology-Renal Physiology 313, no 6 (1 décembre 2017) : F1223—F1231. http://dx.doi.org/10.1152/ajprenal.00697.2016.

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Cystic epithelia acquire mesenchymal-like features in polycystic kidney disease (PKD). In this phenotypic alteration, it is well known that transforming growth factor (TGF)-β/Smad3 signaling is involved; however, there is emerging new data on Smad3 phosphoisoforms: Smad3 phosphorylated at linker regions (pSmad3L), COOH-terminal regions (pSmad3C), and both (pSmad3L/C). pSmad3L/C has a pathological role in colorectal cancer. Mesenchymal phenotype-specific cell responses in the TGF-β/Smad3 pathway are implicated in carcinomas. In this study, we confirmed mesenchymal features and examined Smad3 phosphoisoforms in the cpk mouse, a model of autosomal recessive PKD. Kidney sections were stained with antibodies against mesenchymal markers and domain-specific phospho-Smad3. TGF-β, pSmad3L, pSmad3C, JNK, cyclin-dependent kinase (CDK) 4, and c-Myc were evaluated by Western blotting. Cophosphorylation of pSmad3L/C was assessed by immunoprecipitation. α-Smooth muscle actin, which indicates mesenchymal features, was expressed higher in cpk mice. pSmad3L expression was increased in cpk mice and was predominantly localized in the nuclei of tubular epithelial cells in cysts; however, pSmad3C was equally expressed in both cpk and control mice. Levels of pSmad3L, JNK, CDK4, and c-Myc protein in nuclei were significantly higher in cpk mice than in controls. Immunoprecipitation showed that Smad3 was cophosphorylated (pSmad3L/C) in cpk mice. Smad3 knockout/ cpk double-mutant mice revealed amelioration of cpk abnormalities. These findings suggest that upregulating c-Myc through the JNK/CDK4-dependent pSmad3L pathway may be key to the pathophysiology in cpk mice. In conclusion, a qualitative rather than a quantitative abnormality of the TGF-β/Smad3 pathway is involved in PKD and may be a target for disease-specific intervention.
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13

Pereverzeva, Inna, Elizabeth Whitmire, Bettina Khan et Martine Coué. « Distinct Phosphoisoforms of the XenopusMcm4 Protein Regulate the Function of the Mcm Complex ». Molecular and Cellular Biology 20, no 10 (15 mai 2000) : 3667–76. http://dx.doi.org/10.1128/mcb.20.10.3667-3676.2000.

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ABSTRACT Initiation of DNA replication in eukaryotes requires the assembly of prereplication complexes (pre-Rcs) at the origins of replication. The assembly and function of the pre-Rcs appear to be controlled by phosphorylation events. In this study we report the detailed characterization of the cell cycle phosphorylation of one component of the Xenopus pre-Rcs, the Mcm protein complex. We show that individual Mcm subunits are differentially phosphorylated during the cell cycle. During mitosis, the Mcm4 subunit is hyperphosphorylated, while the other subunits are not actively phosphorylated. The mitotic phosphorylation of Mcm4 requires Cdc2-cyclin B and other unknown kinases. Following exit from mitosis, the Mcm4 subunit of the cytosolic interphase complex undergoes dephosphorylation, and the Mcm2, Mcm3, or Mcm6 subunits are then actively phosphorylated by kinase(s) other than cyclin-dependent kinases (Cdks) or Cdc7. The association of the Mcm complex with the pre-Rcs correlates with the formation of a transient interphase complex. This complex contains an intermediately phosphorylated Mcm4 subunit and is produced by partial dephosphorylation of the mitotic hyperphosphorylated Mcm4 protein. Complete dephosphorylation of the Mcm4 subunit inactivates the Mcm complex and prevents its binding to the chromatin. Once the Mcm complex is assembled on the chromatin the Mcm4 and the Mcm2 proteins are the only subunits phosphorylated during the activation of the pre-Rcs. These chromatin-associated phosphorylations require nuclear transport and are independent of Cdk2-cyclin E. These results suggest that the changes in Mcm4 phosphorylation regulate pre-Rc assembly and the function of the pre-Rcs on the chromatin.
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Pereverzeva, Inna, Elizabeth Whitmire, Bettina Khan et Martine Coué. « Distinct Phosphoisoforms of the XenopusMcm4 Protein Regulate the Function of the Mcm Complex ». Molecular and Cellular Biology 20, no 10 (2000) : 3667–76. http://dx.doi.org/10.1128/.20.10.3667-3676.2000.

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Kim, Seok-Hyung, Soomin Ahn et Cheol-Keun Park. « Smad3 and its phosphoisoforms are prognostic predictors of hepatocellular carcinoma after curative hepatectomy ». Hepatobiliary & ; Pancreatic Diseases International 11, no 1 (février 2012) : 51–59. http://dx.doi.org/10.1016/s1499-3872(11)60125-2.

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de Ancos, J. G., et J. Avila. « Differential distribution in white and grey matter of tau phosphoisoforms containing four tubulin-binding motifs ». Biochemical Journal 296, no 2 (1 décembre 1993) : 351–54. http://dx.doi.org/10.1042/bj2960351.

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The microtubule-associated protein tau has been isolated and purified from both white and grey brain matter. Tau isoforms were fractionated, based on their different phosphate contents, by iron-chelating affinity chromatography. Differences were observed in the proportions of phosphorylated isoforms of tau protein (containing four tubulin-binding motifs) present in white and grey matter. In white matter, isoforms containing four tubulin-binding motifs are mainly present in a phosphorylated form. Thus there appears to be a correlation between the modification, by phosphorylation, of some sites in the tau molecule and the subcellular localization (axonal or somatodendritic compartments) of the modified isoforms.
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Nemec, Corey M., Fan Yang, Joshua M. Gilmore, Corinna Hintermair, Yi-Hsuan Ho, Sandra C. Tseng, Martin Heidemann et al. « Different phosphoisoforms of RNA polymerase II engage the Rtt103 termination factor in a structurally analogous manner ». Proceedings of the National Academy of Sciences 114, no 20 (2 mai 2017) : E3944—E3953. http://dx.doi.org/10.1073/pnas.1700128114.

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The carboxyl-terminal domain (CTD) of the largest subunit of RNA polymerase II (Pol II) orchestrates dynamic recruitment of specific cellular machines during different stages of transcription. Signature phosphorylation patterns of Y1S2P3T4S5P6S7 heptapeptide repeats of the CTD engage specific “readers.” Whereas phospho-Ser5 and phospho-Ser2 marks are ubiquitous, phospho-Thr4 is reported to only impact specific genes. Here, we identify a role for phospho-Thr4 in transcription termination at noncoding small nucleolar RNA (snoRNA) genes. Quantitative proteomics reveals an interactome of known readers as well as protein complexes that were not known to rely on Thr4 for association with Pol II. The data indicate a key role for Thr4 in engaging the machinery used for transcription elongation and termination. We focus on Rtt103, a protein that binds phospho-Ser2 and phospho-Thr4 marks and facilitates transcription termination at protein-coding genes. To elucidate how Rtt103 engages two distinct CTD modifications that are differentially enriched at noncoding genes, we relied on NMR analysis of Rtt103 in complex with phospho-Thr4– or phospho-Ser2–bearing CTD peptides. The structural data reveal that Rtt103 interacts with phospho-Thr4 in a manner analogous to its interaction with phospho-Ser2–modified CTD. The same set of hydrogen bonds involving either the oxygen on phospho-Thr4 and the hydroxyl on Ser2, or the phosphate on Ser2 and the Thr4 hydroxyl, can be formed by rotation of an arginine side chain, leaving the intermolecular interface otherwise unperturbed. This economy of design enables Rtt103 to engage Pol II at distinct sets of genes with differentially enriched CTD marks.
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Mische, Sarah, Yungui He, Lingzhi Ma, Mingang Li, Madeline Serr et Thomas S. Hays. « Dynein Light Intermediate Chain : An Essential Subunit That Contributes to Spindle Checkpoint Inactivation ». Molecular Biology of the Cell 19, no 11 (novembre 2008) : 4918–29. http://dx.doi.org/10.1091/mbc.e08-05-0483.

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The dynein light intermediate chain (LIC) is a subunit unique to the cytoplasmic form of dynein, but how it contributes to dynein function is not fully understood. Previous work has established that the LIC homodimer binds directly to the dynein heavy chain and may mediate the attachment of dynein to centrosomes and other cargoes. Here, we report our characterization of the LIC in Drosophila. Unlike vertebrates, in which two Lic genes encode multiple subunit isoforms, the Drosophila LIC is encoded by a single gene. We determined that the single LIC polypeptide is phosphorylated, and that different phosphoisoforms can assemble into the dynein motor complex. Our mutational analyses demonstrate that, similar to other dynein subunits, the Drosophila LIC is required for zygotic development, germline specification of the oocyte, and mitotic cell division. We show that RNA interference depletion of LIC in Drosophila S2 cells does not block the recruitment of a dynein complex to kinetochores, but it does delay inactivation of Mad2 signaling and mitotic progression. Our observations suggest the LIC contributes to a broad range of dynein functions.
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Pekovic, Vanja, Jens Harborth, Jos L. V. Broers, Frans C. S. Ramaekers, Baziel van Engelen, Martin Lammens, Thomas von Zglinicki, Roland Foisner, Chris Hutchison et Ewa Markiewicz. « Nucleoplasmic LAP2α–lamin A complexes are required to maintain a proliferative state in human fibroblasts ». Journal of Cell Biology 176, no 2 (15 janvier 2007) : 163–72. http://dx.doi.org/10.1083/jcb.200606139.

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In human diploid fibroblasts (HDFs), expression of lamina-associated polypeptide 2 α (LAP2α) upon entry and exit from G0 is tightly correlated with phosphorylation and subnuclear localization of retinoblastoma protein (Rb). Phosphoisoforms of Rb and LAP2α are down-regulated in G0. Although RbS780 phosphoform and LAP2α are up-regulated upon reentry into G1 and colocalize in the nucleoplasm, RbS795 migrates between nucleoplasmic and speckle compartments. In HDFs, which are null for lamins A/C, LAP2α is mislocalized within nuclear aggregates, and this is correlated with cell cycle arrest and accumulation of Rb within speckles. Nuclear retention of nucleoplasmic Rb during G1 phase but not of speckle-associated Rb depends on lamin A/C. siRNA knock down of LAP2α or lamin A/C in HDFs leads to accumulation of Rb in speckles and G1 arrest, probably because of activation of a cell cycle checkpoint. Our results suggest that LAP2α and lamin A/C are involved in controlling Rb localization and phosphorylation, and a lack or mislocalization of either protein leads to cell cycle arrest in HDFs.
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Cechowska-Pasko, Marzanna, et Jerzy Pałka. « Expression of IGF-binding protein-1 phosphoisoforms in fasted rat skin and its role in regulation of collagen biosynthesis ». Comparative Biochemistry and Physiology Part B : Biochemistry and Molecular Biology 134, no 4 (avril 2003) : 703–11. http://dx.doi.org/10.1016/s1096-4959(03)00028-9.

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Dickson, John R., Hyejin Yoon, Matthew P. Frosch et Bradley T. Hyman. « Cytoplasmic Mislocalization of RNA Polymerase II Subunit RPB1 in Alzheimer Disease Is Linked to Pathologic Tau ». Journal of Neuropathology & ; Experimental Neurology 80, no 6 (15 mai 2021) : 530–40. http://dx.doi.org/10.1093/jnen/nlab040.

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Abstract Abnormal protein accumulation and mislocalization is a general hallmark of Alzheimer disease. Recent data suggest nucleocytoplasmic transport may be compromised by tau in Alzheimer disease. In this context, we have examined the RNA polymerase II subunit RPB1, which is the catalytic subunit that plays a critical role in transcription. Using immunofluorescence staining in control and Alzheimer disease hippocampal tissue, we show that 2 phosphoisoforms of RPB1 mislocalize from the nucleus to the cytoplasm of neurons in Alzheimer disease. The number of neurons with this cytoplasmic mislocalization is correlated with the burden of pathologic tau (AT8-immunopositive neurons). In order to test whether there is a causal relationship between pathologic tau and cytoplasmic RPB1 accumulation, we used the rTg4510 mouse model, which expresses a regulatable pathologic human tau species harboring the P301L mutation. Using immunofluorescence staining on brain tissue from young (2.5-month-old) and aged (8.5- to 10-month-old) rTg4510 mice, we found a tau- and age-dependent increase in cytoplasmic mislocalization of Rpb1. In summary, this study provides evidence that tau induces mislocalization of RPB1 in Alzheimer disease, and since RPB1 is essential for transcription, this raises the possibility that RPB1 mislocalization could lead to fundamental alterations in neuronal health.
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Iwashita, M., K. Sakai, Y. Kudo et Y. Takeda. « Phosphoisoforms of insulin-like growth factor binding protein-1 in appropriate-for-gestational-age and small-for-gestational-age fetuses ». Growth Hormone & ; IGF Research 8, no 6 (décembre 1998) : 487–93. http://dx.doi.org/10.1016/s1096-6374(98)80302-x.

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Kajantie, Eero, Leo Dunkel, Eeva-Marja Rutanen, Markku Seppälä, Riitta Koistinen, Annikki Sarnesto et Sture Andersson. « IGF-I, IGF Binding Protein (IGFBP)-3, Phosphoisoforms of IGFBP-1, and Postnatal Growth in Very Low Birth Weight Infants ». Journal of Clinical Endocrinology & ; Metabolism 87, no 5 (mai 2002) : 2171–79. http://dx.doi.org/10.1210/jcem.87.5.8457.

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Mochizuki, T., Y. Katsumata, T. Hoshiai, T. Ozaki, T. Yazaki, M. Iwashita, Y. Nakamura, K. Maruyama et H. Aoki. « Phosphoisoforms of insulin-like growth factor binding protein-1 in appropriate-for-gestational age and small-for-gestational age fetuses ». International Journal of Gynecology & ; Obstetrics 70 (2000) : A78. http://dx.doi.org/10.1016/s0020-7292(00)82743-5.

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Fowler, D., G. Albaiges, C. Lees, J. Jones, K. Nicolaides et J. Miell. « The role of insulin-like growth factor binding protein-1 phosphoisoforms in pregnancies with impaired placental function identified by Doppler ultrasound ». Human Reproduction 14, no 11 (novembre 1999) : 2881–85. http://dx.doi.org/10.1093/humrep/14.11.2881.

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Ciarallo, Sandra, Venkateswaran Subramaniam, Wesley Hung, Jin-Hwa Lee, Rouslan Kotchetkov, Charanjit Sandhu, Andrea Milic et Joyce M. Slingerland. « Altered p27Kip1 Phosphorylation, Localization, and Function in Human Epithelial Cells Resistant to Transforming Growth Factor β-Mediated G1 Arrest ». Molecular and Cellular Biology 22, no 9 (1 mai 2002) : 2993–3002. http://dx.doi.org/10.1128/mcb.22.9.2993-3002.2002.

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ABSTRACT p27Kip1 is an important effector of G1 arrest by transforming growth factor β (TGF-β). Investigations in a human mammary epithelial cell (HMEC) model, including cells that are sensitive (184S) and resistant (184A1L5R) to G1 arrest by TGF-β, revealed aberrant p27 regulation in the resistant cells. Cyclin E1-cyclin-dependent kinase 2 (cdk2) and cyclin A-cdk2 activities were increased, and p27-associated kinase activity was detected in 184A1L5R cells. p27 from 184A1L5R cells was localized to both nucleus and cytoplasm, showed an altered profile of phosphoisoforms, and had a reduced ability to bind and inhibit cyclin E1-cdk2 in vitro when compared to p27 from the sensitive 184S cells. In proliferating 184A1L5R cells, more p27 was associated with cyclin D1-cdk4 complexes than in 184S. While TGF-β inhibited the formation of cyclin D1-cdk4-p27 complexes in 184S cells, it did not inhibit the assembly of cyclin D1-cdk4-p27 complexes in the resistant 184A1L5R cells. p27 phosphorylation changed during cell cycle progression, with cyclin E1-bound p27 in G0 showing a different phosphorylation pattern from that of cyclin D1-bound p27 in mid-G1. These data suggest a model in which TGF-β modulates p27 phosphorylation from its cyclin D1-bound assembly phosphoform to an alternate form that binds tightly to inhibit cyclin E1-cdk2. Altered phosphorylation of p27 in the resistant 184A1L5R cells may favor the binding of p27 to cyclin D1-cdk4 and prevent its accumulation in cyclin E1-cdk2 in response to TGF-β.
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Kajantie, Eero. « Insulin-Like Growth Factor (IGF)-I, IGF Binding Protein (IGFBP)-3, Phosphoisoforms of IGFBP-1 and Postnatal Growth in Very-Low-Birth-Weight Infants ». Hormone Research in Paediatrics 60, no 3 (2003) : 124–30. http://dx.doi.org/10.1159/000074513.

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Hills, F. A., M. G. Elder, T. Chard et M. H. F. Sullivan. « Regulation of human villous trophoblast by insulin-like growth factors and insulin-like growth factor-binding protein-1 ». Journal of Endocrinology 183, no 3 (décembre 2004) : 487–96. http://dx.doi.org/10.1677/joe.1.05867.

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Many studies have implicated the insulin-like growth factors (IGFs) and insulin-like growth factor-binding protein-1 (IGFBP-1) in the control of the feto–maternal interface of human pregnancy, but many of the data are from cell lines derived from primary trophoblast or from extravillous trophoblast. We have obtained highly enriched villous cytotrophoblast (VCT) from first trimester and term human placentae, and investigated the effects of IGF-I, IGF-II and phosphoisoforms of IGFBP-1. First trimester villous trophoblast cells were regulated by all these factors. IGF-II increased cell numbers 3.5-fold after 96 h in culture, and IGF-I had less effect (1.5-fold increase) (both P<0.05). IGF-II also had a greater effect on the levels of matrix metalloproteinase (MMP)-2 and MMP-9. Phosphorylated and non-phosphorylated iso-forms of IGFBP-1 added alone increased cell numbers and MMP levels (P<0.05). IGFBP-1 did not modify the effects of IGF-II on cell numbers or on MMP production. Term VCT numbers and MMP production in vitro were unaffected by IGFs (P>0.05). Cell numbers were increased only by 100 nM IGFBP-1 isoforms (P<0.05), whereas MMP levels released from term cells were optimally increased by 1–10 nM IGFBP-1. Overall, our data show that IGFs regulate only first trimester, but not term, VCT. IGFBP-1 regulates VCT from both gestations, but the effects are concentration and end-point specific. In particular, first trimester cell numbers are more affected by low levels of IGFBP-1, whereas high levels of IGFBP-1 are needed to increase MMP and the converse applies to term VCT; low levels of IGFBP-1 have more effect on MMP levels.
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Martina, N. A. « Gestational Age-Dependent Expression of Insulin-Like Growth Factor-Binding Protein-1 (IGFBP-1) Phosphoisoforms in Human Extraembryonic Cavities, Maternal Serum, and Decidua Suggests Decidua as the Primary Source of IGFBP-1 in these Fluids during Early Pregnancy ». Journal of Clinical Endocrinology & ; Metabolism 82, no 6 (1 juin 1997) : 1894–98. http://dx.doi.org/10.1210/jc.82.6.1894.

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Martina, N. A., E. Kim, U. Chitkara, N. C. Wathen, T. Chard et L. C. Giudice. « Gestational Age-Dependent Expression of Insulin-Like Growth Factor-Binding Protein-1 (IGFBP-1) Phosphoisoforms in Human Extraembryonic Cavities, Maternal Serum, and Decidua Suggests Decidua as the Primary Source of IGFBP-1 in these Fluids during Early Pregnancy1 ». Journal of Clinical Endocrinology & ; Metabolism 82, no 6 (1 juin 1997) : 1894–98. http://dx.doi.org/10.1210/jcem.82.6.3974.

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Cho, Soo Youn, Sang Yun Ha, Song-Mei Huang, Jeong Hoon Kim, Myung Soo Kang, Hae-yong Yoo, Hyeon-ho Kim et al. « The prognostic significance of Smad3, Smad4, Smad3 phosphoisoform expression in esophageal squamous cell carcinoma ». Medical Oncology 31, no 11 (30 septembre 2014). http://dx.doi.org/10.1007/s12032-014-0236-9.

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Tahashi, Yoshiya, Koichi Matsuzaki, Kazuichi Okazaki, Shigeo Mori, Katsunori Yoshida, Hideo Yamagata, Miki Murata et al. « Involvement of Smad3 phosphoisoform-mediated signaling in the development of colonic cancer in IL-10-deficient mice ». International Journal of Oncology, 1 juin 2008. http://dx.doi.org/10.3892/ijo.32.6.1221.

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Dory, Magdalena, Zoltán Doleschall, Szilvia K. Nagy, Helga Ambrus, Tamás Mészáros, Beáta Barnabás et Róbert Dóczi. « Kinase-Associated Phosphoisoform Assay : a novel candidate-based method to detect specific kinase-substrate phosphorylation interactions in vivo ». BMC Plant Biology 16, no 1 (21 septembre 2016). http://dx.doi.org/10.1186/s12870-016-0894-1.

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Bańkowski, Edward, Krzysztof Sobolewski, Jerzy Palka et Stefan Jaworski. « Decreased expression of the insulin-like growth factor-I-binding protein-1 (IGFBP-1) phosphoisoform in pre-eclamptic Wharton's jelly and its role in the regulation of collagen biosynthesis ». Clinical Chemistry and Laboratory Medicine (CCLM) 42, no 2 (18 janvier 2004). http://dx.doi.org/10.1515/cclm.2004.032.

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AbstractInsulin-like growth factor-I (IGF-I) is known as an important stimulator of collagen and glycosaminoglycans (GAGs) biosynthesis in tissues. IGF-I activity is under control of IGF-I-binding proteins (IGFBPs) with different IGF-I-binding affinity. IGFBP-1 is known as an inhibitor of IGF-dependent functions. Some IGFBPs (e.g., IGFBP-1) may undergo phosphorylation that dramatically increases IGFBP affinity for IGF. Wharton's jelly represents a reservoir of IGF-I and its binding proteins (BPs). Pre-eclampsia, the most common, pregnancy-associated pathological syndrome, contributes to a significant decrease in IGF-I and IGFBP-1 content in Wharton's jelly, although it does not affect collagen content in this tissue. In the present study we show that control Wharton's jelly contains phosphorylated forms of IGFBP-1 that are dramatically dephosphorylated during pre-eclampsia. A dramatic decrease in IGF-I binding to immunoprecipitated IGFBP-1 from pre-eclamptic Wharton's jelly compared to the control was observed. Western immunoblot analysis with anti-phosphothreonine antibodies for immunoprecipitated IGFBP-1 from control and pre-eclamptic Wharton's jelly revealed that both tissues contain phosphorylated forms of IGFBP-1. However, a distinct decrease in the expression of phosphorylated IGFBP-1 from pre-eclamptic Wharton's jelly was observed. The functional significance of the phenomenon was found in cultured fibroblasts treated with IGFBP isolated from Wharton's jelly extracts. A significant decrease in collagen biosynthesis was found in the cells treated with IGFBP of control Wharton's jelly, while in the presence of IGFBP from pre-eclamptic Wharton's jelly, the rate of collagen biosynthesis was similar to that in the control cells. The result was corroborated by data showing increase in expression of IGF-I receptor and phosphorylated MAP kinases (ERK1 and ERK2) in fibroblasts cultured in the presence of IGFBP from pre-eclamptic Wharton's jelly, compared to control. The data suggest that the decrease in phosphorylated IGFBP-1 in pre-eclamptic Wharton's jelly may decrease IGF-I-binding affinity for IGF and increase the bioavailability of IGF-I for receptor interaction. This mechanism may facilitate IGF-I-dependent stimulation of fibroblasts to produce extracellular matrix (ECM) components even at a low IGF-I tissue level. Therefore, IGFBP-1 phosphoisoforms in Wharton's jelly may play an important role in the regulation of IGF-I-dependent functions during pre-eclampsia.
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Weber, Martina, Jeffrey P. Moore et Charles D. Searles. « Abstract 255 : Laminar Shear Stress Enhances the Activity and Localization of RNA Polymerase II on the eNOS Gene ». Circulation 116, suppl_16 (16 octobre 2007). http://dx.doi.org/10.1161/circ.116.suppl_16.ii_30-d.

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We have previously found that laminar shear enhances eNOS mRNA stability and translation by altering endothelial NO synthase (eNOS) mRNA 3′ polyadenylation. Transcription is tightly coupled to pre-mRNA processing, and is coordinated by RNA polymerase (RNAP) II. We assessed whether laminar shear stress alters the activity and localization of RNAP II on the eNOS gene. We found that endothelial cells exposed to laminar shear stress had a 2-fold (n=3, p < 0.05) increase in total RNAP II protein levels compared to control; this effect was dose-dependent (0–15 dynes/cm2). Since three different RNAP II phosphoisoforms are associated with different stages of mRNA synthesis, we examined whether shear stress affected protein expression of these particular phosphoisoforms. We found that cells exposed to laminar shear had a 3-fold increase (p<0.05) in expression of RNAP II phosphorylated at serine 2, which is associated with transcription elongation and 3′ polyadenylation. In contrast, shear stress did not alter expression of the other phosphoisoforms. We performed chromatin immunoprecipitation (ChIP) analysis to examine shear-induced changes in RNAP II localization on the eNOS gene. Using antibody against total RNAP II, eNOS sequences along the entire gene were amplified. Using the phosphoserine 2 specific RNAP II antibody, we found active RNAP II predominantly bound to the 3′UTR (exon 26) and downstream sequence of eNOS in sheared cells. These findings were confirmed by quantitative ChIP (3 fold increase, n = 8, p = 0.0378). This suggests that shear-induced changes in RNAP II phosphorylation enhance its ability to polyadenylate eNOS mRNA. Serine 2 phosphorylation is dependent on cyclin-dependent kinase 9 (CDK 9), and shear-induced recruitment of CDK 9 to the eNOS gene was examined. We found that endothelial cells exposed to laminar shear had enhanced localization of CDK 9 to the eNOS promoter and exons 8 and 22, and diminished localizationto exon 26 and in the downstream sequence. This indicates that shear recruits CDK 9 while RNAP II is bound to the promoter and early exons to activate RNAP by phosphorylating serine 2. In conclusion, laminar shear stress enhances eNOS mRNA processing and increases gene expression through recruitment of CDK 9 and activation of RNAP II.
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Schenk, Christian, Max Meyrath, Uwe Warnken, Martina Schnölzer, Walter Mier, Christian Harak et Volker Lohmann. « Characterization of a Threonine-Rich Cluster in Hepatitis C Virus Nonstructural Protein 5A and Its Contribution to Hyperphosphorylation ». Journal of Virology 92, no 24 (26 septembre 2018). http://dx.doi.org/10.1128/jvi.00737-18.

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ABSTRACTHepatitis C virus (HCV) nonstructural protein 5A (NS5A) is a phosphoprotein with key functions in regulating viral RNA replication and assembly. Two phosphoisoforms are discriminated by their different apparent molecular weights: a basally phosphorylated (p56) and a hyperphosphorylated (p58) variant. The precise mechanisms governing p58 synthesis and specific functions of the isoforms are poorly understood. Our study aimed at a deeper understanding of determinants involved in p58 synthesis. We analyzed two variants of p56 and p58 of isolate JFH-1 separately by mass spectrometry using an expression model and thereby identified a threonine-rich phosphopeptide exclusively found in the hyperphosphorylated variant. Individual exchange of possible phosphoacceptor sites to phosphoablatant or -mimetic residues had little impact on HCV replication or assembly in cell culture. A phosphospecific antibody recognizing pT242 revealed that this position was indeed phosphorylated only in p58 and depended on casein kinase Iα. Importantly, phosphoablative mutations at positions T244 and S247 abrogated pT242 detection without substantial effects on global p58 levels, whereas mutations in the preceding serine-rich cluster dramatically reduced total p58 levels but had minor impact on pT242 levels, suggesting the existence of distinct subspecies of hyperphosphorylated NS5A. Mass spectrometry analyses of different genotypes showed variable phosphorylation patterns across NS5A and suggested that the threonine-rich region is also phosphorylated at T242 in gt4a and at S249 in gt1a, gt1b, and gt4a. Our data therefore indicate that p58 is not a single homogenously phosphorylated protein species but rather a population of various phosphoisoforms, with high variability between genotypes.IMPORTANCEHepatitis C virus infections affect 71 million people worldwide and cause severe chronic liver disease. Recently, efficient antiviral therapies have been established, with inhibitors of nonstructural protein NS5A as a cornerstone. NS5A is a central regulator of HCV replication and assembly but is still enigmatic in its molecular functions. It exists in two phosphoisoforms, p56 and p58. We identified a phosphopeptide exclusively found in p58 and analyzed the determinants involved in phosphorylation of this region. We found evidence for very different phosphorylation patterns resulting in p58. These results challenge the concept of p58 being a homogenous species of NS5A molecules phosphorylated at the same positions and argues for at least two independently phosphorylated variants showing the same electrophoretic mobility, likely serving different functions.
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