Artículos de revistas: "SERBP1"

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Lee, Yu-Jen, Hung-Ming Wei, Ling-Yun Chen y Chuan Li. "Localization of SERBP1 in stress granules and nucleoli". FEBS Journal 281, n.º 1 (9 de diciembre de 2013): 352–64. http://dx.doi.org/10.1111/febs.12606.

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Bashour, Nicholas Michael y Susan Wray. "Progesterone Directly and Rapidly Inhibits GnRH Neuronal Activity via Progesterone Receptor Membrane Component 1". Endocrinology 153, n.º 9 (1 de septiembre de 2012): 4457–69. http://dx.doi.org/10.1210/en.2012-1122.

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GnRH neurons are essential for reproduction, being an integral component of the hypothalamic-pituitary-gonadal axis. Progesterone (P4), a steroid hormone, modulates reproductive behavior and is associated with rapid changes in GnRH secretion. However, a direct action of P4 on GnRH neurons has not been previously described. Receptors in the progestin/adipoQ receptor family (PAQR), as well as progesterone receptor membrane component 1 (PgRMC1) and its partner serpin peptidase inhibitor, clade E (nexin, plasminogen activator inhibitor type 1) mRNA binding protein 1 (SERBP1), have been shown to mediate rapid progestin actions in various tissues, including the brain. This study shows that PgRMC1 and SERBP1, but not PAQR, are expressed in prenatal GnRH neurons. Expression of PgRMC1 and SERBP1 was verified in adult mouse GnRH neurons. To investigate the effect of P4 on GnRH neuronal activity, calcium imaging was used on primary GnRH neurons maintained in explants. Application of P4 significantly decreased the activity of GnRH neurons, independent of secretion of gamma-aminobutyric acidergic and glutamatergic input, suggesting a direct action of P4 on GnRH neurons. Inhibition was not blocked by RU486, an antagonist of the classic nuclear P4 receptor. Inhibition was also maintained after uncoupling of the inhibitory regulative G protein (Gi/o), the signal transduction pathway used by PAQR. However, AG-205, a PgRMC1 ligand and inhibitor, blocked the rapid P4-mediated inhibition, and inhibition of protein kinase G, thought to be activated downstream of PgRMC1, also blocked the inhibitory activity of P4. These data show for the first time that P4 can act directly on GnRH neurons through PgRMC1 to inhibit neuronal activity.

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Mari, Yelenis, Graham M. West, Catherina Scharager-Tapia, Bruce D. Pascal, Ruben D. Garcia-Ordonez y Patrick R. Griffin. "SERBP1 Is a Component of the Liver Receptor Homologue-1 Transcriptional Complex". Journal of Proteome Research 14, n.º 11 (7 de octubre de 2015): 4571–80. http://dx.doi.org/10.1021/acs.jproteome.5b00379.

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4

Bolger, Graeme B. "The RNA-binding protein SERBP1 interacts selectively with the signaling protein RACK1". Cellular Signalling 35 (julio de 2017): 256–63. http://dx.doi.org/10.1016/j.cellsig.2017.03.001.

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5

Wang, Ting, Ling Xu, Rongrong Jia y Jue Wei. "MiR-218 suppresses the metastasis and EMT of HCC cells via targeting SERBP1". Acta Biochimica et Biophysica Sinica 49, n.º 5 (20 de marzo de 2017): 383–91. http://dx.doi.org/10.1093/abbs/gmx017.

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6

Wang, Zhenchang, DanDan Huang, Jingjing Huang, Kunmei Nie, Xiaofan Li y Xiaojin Yang. "lncRNA TMPO-AS1 Exerts Oncogenic Roles in HCC Through Regulating miR-320a/SERBP1 Axis". OncoTargets and Therapy Volume 13 (julio de 2020): 6539–51. http://dx.doi.org/10.2147/ott.s250355.

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7

Muto, Akiko, Yoshihiko Sugihara, Minami Shibakawa, Kenzi Oshima, Tsukasa Matsuda y Daita Nadano. "The mRNA-binding protein Serbp1 as an auxiliary protein associated with mammalian cytoplasmic ribosomes". Cell Biochemistry and Function 36, n.º 6 (23 de julio de 2018): 312–22. http://dx.doi.org/10.1002/cbf.3350.

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8

Lee, Yu-Jen, Wan-Yu Hsieh, Ling-Yun Chen y Chuan Li. "Protein arginine methylation of SERBP1 by protein arginine methyltransferase 1 affects cytoplasmic/nuclear distribution". Journal of Cellular Biochemistry 113, n.º 8 (15 de junio de 2012): 2721–28. http://dx.doi.org/10.1002/jcb.24151.

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9

Ahn, Jang-Won, Sunjik Kim, Wooju Na, Su-Jin Baek, Jeong-Hwan Kim, Keehong Min, Jeonghun Yeom et al. "SERBP1 affects homologous recombination-mediated DNA repair by regulation of CtIP translation during S phase". Nucleic Acids Research 43, n.º 13 (11 de junio de 2015): 6321–33. http://dx.doi.org/10.1093/nar/gkv592.

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Salsano, Stefania, Alicia Quiñonero, Silvia Pérez, Tamara Garrido Gómez, Carlos Simón y Francisco Dominguez. "Dynamic expression of PGRMC1 and SERBP1 in human endometrium: an implication in the human decidualization process". Fertility and Sterility 108, n.º 5 (noviembre de 2017): 832–42. http://dx.doi.org/10.1016/j.fertnstert.2017.07.1163.

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11

KOENSGEN, D., A. MUSTEA, I. KLAMAN, P. SUN, M. ZAFRAKAS, W. LICHTENEGGER, C. DENKERT, E. DAHL y J. SEHOULI. "Expression analysis and RNA localization of PAI-RBP1 (SERBP1) in epithelial ovarian cancer: Association with tumor progression". Gynecologic Oncology 107, n.º 2 (noviembre de 2007): 266–73. http://dx.doi.org/10.1016/j.ygyno.2007.06.023.

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12

Colleti, Carolina, Talita Diniz Melo-Hanchuk, Flávia Regina Moraes da Silva, Ângela Saito y Jörg Kobarg. "Complex interactomes and post-translational modifications of the regulatory proteins HABP4 and SERBP1 suggest pleiotropic cellular functions". World Journal of Biological Chemistry 10, n.º 3 (21 de noviembre de 2019): 44–64. http://dx.doi.org/10.4331/wjbc.v10.i3.44.

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13

Guo, Kai, Shaobo Zheng, Yawen Xu, Abai Xu, Binshen Chen y Yong Wen. "Loss of miR-26a-5p promotes proliferation, migration, and invasion in prostate cancer through negatively regulating SERBP1". Tumor Biology 37, n.º 9 (23 de julio de 2016): 12843–54. http://dx.doi.org/10.1007/s13277-016-5158-z.

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14

Li, GuoYong, Peng Du, JianPeng He y Yong Li. "CircRNA circBACH1 (hsa_circ_0061395) serves as a miR-656–3p sponge to facilitate hepatocellular carcinoma progression through increasing SERBP1 expression". Biochemical and Biophysical Research Communications 556 (junio de 2021): 1–8. http://dx.doi.org/10.1016/j.bbrc.2021.03.136.

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15

Chew, Ting Gang, Anne Peaston, Ai Khim Lim, Chanchao Lorthongpanich, Barbara B. Knowles y Davor Solter. "A Tudor Domain Protein SPINDLIN1 Interacts with the mRNA-Binding Protein SERBP1 and Is Involved in Mouse Oocyte Meiotic Resumption". PLoS ONE 8, n.º 7 (22 de julio de 2013): e69764. http://dx.doi.org/10.1371/journal.pone.0069764.

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16

Hao, Ruihu, Haiwei Du, Lin Guo, Fengde Tian, Ning An, Tiejun Yang, Changcheng Wang, Bo Wang y Zihao Zhou. "Identification of dysregulated genes in rheumatoid arthritis based on bioinformatics analysis". PeerJ 5 (15 de marzo de 2017): e3078. http://dx.doi.org/10.7717/peerj.3078.

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BackgroundRheumatoid arthritis (RA) is a chronic auto-inflammatory disorder of joints. The present study aimed to identify the key genes in RA for better understanding the underlying mechanisms of RA.MethodsThe integrated analysis of expression profiling was conducted to identify differentially expressed genes (DEGs) in RA. Moreover, functional annotation, protein–protein interaction (PPI) network and transcription factor (TF) regulatory network construction were applied for exploring the potential biological roles of DEGs in RA. In addition, the expression level of identified candidate DEGs was preliminarily detected in peripheral blood cells of RA patients in theGSE17755dataset. Quantitative real-time polymerase chain reaction (qRT-PCR) was conducted to validate the expression levels of identified DEGs in RA.ResultsA total of 378 DEGs, including 202 up- and 176 down-regulated genes, were identified in synovial tissues of RA patients compared with healthy controls. DEGs were significantly enriched in axon guidance, RNA transport and MAPK signaling pathway. RBFOX2, LCK and SERBP1 were the hub proteins in the PPI network. In the TF-target gene network, RBFOX2, POU6F1, WIPF1 and PFKFB3 had the high connectivity with TFs. The expression status of 11 candidate DEGs was detected inGSE17755, the expression levels of MAT2A and NSA2 were significantly down-regulated and CD47 had the up-regulated tendency in peripheral blood cells of patients with RA compared with healthy individuals. qRT-PCR results of MAT2A, NSA2, CD47 were compatible with our bioinformatics analyses.DiscussionOur study might provide valuable information for exploring the pathogenesis mechanism of RA and identifying the potential biomarkers for RA diagnosis.

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17

Forde, N., G. B. Duffy, P. A. McGettigan, J. A. Browne, J. P. Mehta, A. K. Kelly, N. Mansouri-Attia et al. "Evidence for an early endometrial response to pregnancy in cattle: both dependent upon and independent of interferon tau". Physiological Genomics 44, n.º 16 (15 de agosto de 2012): 799–810. http://dx.doi.org/10.1152/physiolgenomics.00067.2012.

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The aims of this study were to 1) identify the earliest transcriptional response of the bovine endometrium to the presence of the conceptus (using RNAseq), 2) investigate if these genes are regulated by interferon tau (IFNT) in vivo, and 3) determine if they are predictive of the pregnancy status of postpartum dairy cows. RNAseq identified 459 differentially expressed genes (DEGs) between pregnant and cyclic endometria on day 16. Quantitative real-time PCR analysis of selected genes revealed PARP12, ZNFX1, HERC6, IFI16, RNF213, and DDX58 expression increased in pregnant compared with cyclic endometria on day 16 and were directly upregulated by intrauterine infusion of IFNT in vivo for 2 h ( P < 0.05). On day 13 following estrous endometrial expression of nine genes increased [ ARHGAP1, MGC127874, LIMS2, TBC1D1, FBXL7, C25H16orf71, LOC507810, ZSWIM4, and one novel gene (ENSBTAT00000050193)] and seven genes decreased ( SERBP1, SRGAP2, AL7A1, TBK1, F2RL2, MGC128929, and WBSCR17; P < 0.05) in pregnant compared with cyclic heifers. Of these DEGs, significant differences in expression between pregnant and cyclic endometria were maintained on day 16 for F2RL2, LIMS2, LOC507810, MGC127874, TBC1D1, WBSCR17, and ZSWIM4 ( P < 0.05) both their expression was not directly regulated by IFNT in vivo. Analysis of the expression of selected interferon-stimulated genes in blood samples from postpartum dairy cows revealed a significant increase ( P < 0.05) in expression of ZXFX1, PARP12, SAMD9, and HERC6 on day 18 following artificial insemination in cows subsequently confirmed pregnant compared with cyclic controls. In conclusion, RNAseq identified a number of novel pregnancy-associated genes in the endometrium of cattle during early pregnancy that are not regulated by IFNT in vivo. In addition, a number of genes that are directly regulated by short term exposure to IFNT in vivo are differentially expressed on day 18 following estrus detection in the blood of postpartum dairy cows depending on their pregnancy status.

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18

Hori, Osamu, Mayuki Miyazaki, Takashi Tamatani, Kentaro Ozawa, Katsura Takano, Masaru Okabe, Masahito Ikawa et al. "Deletion of SERP1/RAMP4, a Component of the Endoplasmic Reticulum (ER) Translocation Sites, Leads to ER Stress". Molecular and Cellular Biology 26, n.º 11 (1 de junio de 2006): 4257–67. http://dx.doi.org/10.1128/mcb.02055-05.

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ABSTRACT Stress-associated endoplasmic reticulum (ER) protein 1 (SERP1), also known as ribosome-associated membrane protein 4 (RAMP4), is a Sec61-associated polypeptide that is induced by ER stress. SERP1−/− mice, made by targeted gene disruption, demonstrated growth retardation, increased mortality, and impaired glucose tolerance. Consistent with high levels of SERP1 expression in pancreas, pancreatic islets from SERP1−/− mice failed to rapidly synthesize proinsulin in response to a glucose load. In addition, reduced size and enhanced ER stress were observed in the anterior pituitary of SERP1−/− mice, and growth hormone production was slowed in SERP1−/− pituitary after insulin stimulation. Experiments using pancreatic microsomes revealed aberrant association of ribosomes and the Sec61 complex and enhanced ER stress in SERP1−/− pancreas. In basal conditions, the Sec61 complex in SERP1−/− microsomes was more cofractionated with ribosomes, compared with SERP1+/+ counterparts, in high-salt conditions. In contrast, after glucose stimulation, the complex showed less cofractionation at an early phase (45 min) but more at a later phase (120 min). Although intracellular insulin/proinsulin levels were not significantly changed in both genotypes, these results suggest that subtle changes in translocation efficiency play an important role in the regulation of ER stress and rapid polypeptide synthesis.

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Yamaguchi, Atsushi, Osamu Hori, David M. Stern, Enno Hartmann, Satoshi Ogawa y Masaya Tohyama. "Stress-Associated Endoplasmic Reticulum Protein 1 (Serp1)/Ribosome-Associated Membrane Protein 4 (Ramp4) Stabilizes Membrane Proteins during Stress and Facilitates Subsequent Glycosylation". Journal of Cell Biology 147, n.º 6 (13 de diciembre de 1999): 1195–204. http://dx.doi.org/10.1083/jcb.147.6.1195.

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Application of differential display to cultured rat astrocytes subjected to hypoxia allowed cloning of a novel cDNA, termed stress-associated endoplasmic reticulum protein 1 (SERP1). Expression of SERP1 was enhanced in vitro by hypoxia and/or reoxygenation or other forms of stress, causing accumulation of unfolded proteins in endoplasmic reticulum (ER) stress, and in vivo by middle cerebral artery occlusion in rats. The SERP1 cDNA encodes a 66–amino acid polypeptide which was found to be identical to ribosome-associated membrane protein 4 (RAMP4) and bearing 29% identity to yeast suppressor of SecY 6 protein (YSY6p), suggesting participation in pathways controlling membrane protein biogenesis at ER. In cultured 293 cells subjected to ER stress, overexpression of SERP1/RAMP4 suppressed aggregation and/or degradation of newly synthesized integral membrane proteins, and subsequently, facilitated their glycosylation when the stress was removed. SERP1/RAMP4 interacted with Sec61α and Sec61β, which are subunits of translocon, and a molecular chaperon calnexin. Furthermore, Sec61α and Sec61β, but not SERP1/RAMP4, were found to associate with newly synthesized integral membrane proteins under stress. These results suggest that stabilization of membrane proteins in response to stress involves the concerted action of a rescue unit in the ER membrane comprised of SERP1/RAMP4, other components of translocon, and molecular chaperons in ER.

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20

Tian, Jia-Ni, Chi-Chen Yang, Chiu-Kai Chuang, Ming-Han Tsai, Ren-Huang Wu, Chiung-Tong Chen y Andrew Yueh. "A Dengue Virus Type 2 (DENV-2) NS4B-Interacting Host Factor, SERP1, Reduces DENV-2 Production by Suppressing Viral RNA Replication". Viruses 11, n.º 9 (27 de agosto de 2019): 787. http://dx.doi.org/10.3390/v11090787.

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Host cells infected with dengue virus (DENV) often trigger endoplasmic reticulum (ER) stress, a key process that allows viral reproduction, without killing the host cells until the late stage of the virus life-cycle. However, little is known regarding which DENV viral proteins interact with the ER machinery to support viral replication. In this study, we identified and characterized a novel host factor, stress-associated ER protein 1 (SERP1), which interacts with the DENV type 2 (DENV-2) NS4B protein by several assays, for example, yeast two-hybrid, subcellular localization, NanoBiT complementation, and co-immunoprecipitation. A drastic increase (34.5-fold) in the SERP1 gene expression was observed in the DENV-2-infected or replicon-transfected Huh7.5 cells. The SERP1 overexpression inhibited viral yields (37-fold) in the DENV-2-infected Huh7.5 cells. In contrast, shRNAi-knockdown and the knockout of SERP1 increased the viral yields (3.4- and 16-fold, respectively) in DENV-2-infected HEK-293 and Huh7.5 cells, respectively. DENV-2 viral RNA replication was severely reduced in stable SERP1-expressing Huh7.5 cells transfected with DENV-2 replicon plasmids. The overexpression of DENV-2 NS4B alleviated the inhibitory effect of SERP1 on DENV-2 RNA replication. Taking these results together, we hypothesized that SERP1 may serve as an antiviral player during ER stress to restrict DENV-2 infection. Our studies revealed novel anti-DENV drug targets that may facilitate anti-DENV drug discovery.

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Jung, Sunmin, Junho Hyun, Jihoon Nah, Jonghee Han, Seo-Hyun Kim, Jaesang Park, Yoonseo Oh et al. "SERP1 is an assembly regulator of γ-secretase in metabolic stress conditions". Science Signaling 13, n.º 623 (17 de marzo de 2020): eaax8949. http://dx.doi.org/10.1126/scisignal.aax8949.

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The enzyme γ-secretase generates β-amyloid (Aβ) peptides by cleaving amyloid protein precursor (APP); the aggregation of these peptides is associated with Alzheimer’s disease (AD). Despite the development of various γ-secretase regulators, their clinical use is limited by coincident disruption of other γ-secretase–regulated substrates, such as Notch. Using a genome-wide functional screen of γ-secretase activity in cells and a complementary DNA expression library, we found that SERP1 is a previously unknown γ-secretase activator that stimulates Aβ generation in cells experiencing endoplasmic reticulum (ER) stress, such as is seen with diabetes. SERP1 interacted with a subcomplex of γ-secretase (APH1A/NCT) through its carboxyl terminus to enhance the assembly and, consequently, the activity of the γ-secretase holoenzyme complex. In response to ER stress, SERP1 preferentially recruited APP rather than Notch into the γ-secretase complex and enhanced the subcellular localization of the complex into lipid rafts, increasing Aβ production. Moreover, SERP1 abundance, γ-secretase assembly, and Aβ production were increased both in cells exposed to high amounts of glucose and in diabetic AD model mice. Conversely, Aβ production was decreased by knocking down SERP1 in cells or in the hippocampi of mice. Compared to postmortem samples from control individuals, those from patients with AD showed increased SERP1 expression in the hippocampus and parietal lobe. Together, our findings suggest that SERP1 is an APP-biased regulator of γ-secretase function in the context of cell stress, providing a possible molecular explanation for the link between diabetes and sporadic AD.

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Guo, Shulong, Shaoya Wang, Youxiao Zeng y Qiaosheng Hu. "Stress-Associated Endoplasmic Reticulum Protein 1 Protected High Glucose-Induced Islet β Cells from Apoptosis by Attenuating Endoplasmic Reticulum Stress". Journal of Biomaterials and Tissue Engineering 9, n.º 12 (1 de diciembre de 2019): 1731–38. http://dx.doi.org/10.1166/jbt.2019.2192.

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The incidence of type II diabetes caused by islet cell injury is increasing in recent years. Endoplasmic reticulum stress is one of the crucial causes of islet β cell damage, and stress-associated endoplasmic reticulum protein 1 (SERP1) could inhibit the occurrence and development of endoplasmic reticulum stress. But whether SERP1 could inhibit the damage of islet β cell caused by endoplasmic reticulum stress is unclear. In this study, we detected the levels of SERP1 and endoplasmic reticulum stress related proteins (p-PERK, p-Eif2 α, ATF-4 and CHOP) by western blotting. Next the lentivirus was used to construct the islet cell line which was stable overexpressed SERP1. Then the expression of endoplasmic reticulum stress related proteins and inflammatory factors was determined with western blotting. At last the apoptosis rates of islet β cells were detected by flow cytometry. We found that high glucose medium promoted the expression of p-PERK, p-Eif2 α, ATF-4 and CHOP while downregulated the levels of SERP1 in isletβ cells. Moreover, overexpression of SERP1 induced the downregulation of levels of p-PERK, p-Eif2 α, ATF-4, CHOP, TNF-α , IL-1β and IL-6 and alleviated the apoptosis of islet cells. At last, the overexpression of CHOP rescued the apoptosis rates and the expression of TNF-α, IL-1β and IL-6. These results indicated SERP1 relieved the inflammation response and apoptosis of islet β cells by inhibiting the expression of CHOP and alleviating the endoplasmic reticulum stress induced damage.

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Miedlich, Susanne U. y Abdul B. Abou-Samra. "Eliminating phosphorylation sites of the parathyroid hormone receptor type 1 differentially affects stimulation of phospholipase C and receptor internalization". American Journal of Physiology-Endocrinology and Metabolism 295, n.º 3 (septiembre de 2008): E665—E671. http://dx.doi.org/10.1152/ajpendo.00036.2008.

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The parathyroid hormone (PTH)/PTH-related peptide (PTHrP) receptor (PTH1R) belongs to family B of seven-transmembrane-spanning receptors and is activated by PTH and PTHrP. Upon PTH stimulation, the rat PTH1R becomes phosphorylated at seven serine residues. Elimination of all PTH1R phosphorylation sites results in prolonged cAMP accumulation and impaired internalization in stably transfected LLC-PK1 cells. The present study explores the role of individual PTH1R phosphorylation sites in PTH1R signaling through phospholipase C, agonist-dependent receptor internalization, and regulation by G protein-coupled receptor kinases. By means of transiently transfected COS-7 cells, we demonstrate that the phosphorylation-deficient (pd) PTH1R confers dramatically enhanced coupling to Gq/11 proteins upon PTH stimulation predominantly caused by elimination of Ser491/492/493, Ser501, or Ser504. Reportedly, impaired internalization of the pd PTH1R, however, is not dependent on a specific phosphorylation site. In addition, we show that G protein-coupled receptor kinase 2 interferes with pd PTH1R signaling to Gq/11 proteins at least partially by direct binding to Gq/11 proteins.

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Kowalik, Magdalena K., Dominika Slonina, Robert Rekawiecki y Jan Kotwica. "Expression of progesterone receptor membrane component (PGRMC) 1 and 2, serpine mRNA binding protein 1 (SERBP1) and nuclear progesterone receptor (PGR) in the bovine endometrium during the estrous cycle and the first trimester of pregnancy". Reproductive Biology 13, n.º 1 (marzo de 2013): 15–23. http://dx.doi.org/10.1016/j.repbio.2013.01.170.

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Noens, Elke E. E. y Juke S. Lolkema. "Physiology and Substrate Specificity of Two Closely Related Amino Acid Transporters, SerP1 and SerP2, of Lactococcus lactis". Journal of Bacteriology 197, n.º 5 (22 de diciembre de 2014): 951–58. http://dx.doi.org/10.1128/jb.02471-14.

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TheserP1andserP2genes found adjacently on the chromosome ofLactococcus lactisstrains encode two members of the amino acid-polyamine-organocation (APC) superfamily of secondary transporters that share 61% sequence identity. SerP1 transportsl-serine,l-threonine, andl-cysteine with high affinity. Affinity constants (Km) are in the 20 to 40 μM range. SerP2 is adl-alanine/dl-serine/glycine transporter. The preferred substrate appears to bedl-alanine for which the affinities were found to be 38 and 20 μM for thedandlisomers, respectively. The common substratel-serine is a high-affinity substrate of SerP1 and a low-affinity substrate of SerP2 with affinity constants of 18 and 356 μM, respectively. Growth experiments demonstrate that SerP1 is the mainl-serine transporter responsible for optimal growth in media containing free amino acids as the sole source of amino acids. SerP2 is able to replace SerP1 in this role only in medium lacking the high-affinity substratesl-alanine and glycine. SerP2 plays an adverse role for the cell by being solely responsible for the uptake of toxicd-serine. The main function of SerP2 is in cell wall biosynthesis through the uptake ofd-alanine, an essential precursor in peptidoglycan synthesis. SerP2 has overlapping substrate specificity and shares 42% sequence identity with CycA ofEscherichia coli, a transporter whose involvement in peptidoglycan synthesis is well established. No evidence was obtained for a role of SerP1 and SerP2 in the excretion of excess amino acids during growth ofL. lactison protein/peptide-rich media.

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Gao, Min, Tianyi Yu, Dan Liu, Yan Shi, Peilang Yang, Jie Zhang, Jizhuang Wang, Yan Liu y Xiong Zhang. "Sepsis plasma-derived exosomal miR-1-3p induces endothelial cell dysfunction by targeting SERP1". Clinical Science 135, n.º 2 (enero de 2021): 347–65. http://dx.doi.org/10.1042/cs20200573.

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Abstract Acute lung injury (ALI) is the leading cause of death in sepsis patients. Exosomes participate in the occurrence and development of ALI by regulating endothelial cell inflammatory response, oxidative stress and apoptosis, causing serious pulmonary vascular leakage and interstitial edema. The current study investigated the effect of exosomal miRNAs on endothelial cells during sepsis. We found a significant increase in miR-1-3p expression in cecal ligation and puncture (CLP) rats exosomes sequencing and sepsis patients’ exosomes, and lipopolysaccharide (LPS)-stimulated human umbilical vein endothelial cells (HUVECs) in vitro. However, the specific biological function of miR-1-3p in ALI remains unknown. Therefore, mimics or inhibitors of miR-1-3p were transfected to modulate its expression in HUVECs. Cell proliferation, apoptosis, contraction, permeability, and membrane injury were examined via cell counting kit-8 (CCK-8), flow cytometry, phalloidin staining, Transwell assay, lactate dehydrogenase (LDH) activity, and Western blotting. The miR-1-3p target gene was predicted with miRNA-related databases and validated by luciferase reporter. Target gene expression was blocked by siRNA to explore the underlying mechanisms. The results illustrated increased miR-1-3p and decreased stress-associated endoplasmic reticulum protein 1 (SERP1) expression both in vivo and in vitro. SERP1 was a direct target gene of miR-1-3p. Up-regulated miR-1-3p inhibits cell proliferation, promotes apoptosis and cytoskeleton contraction, increases monolayer endothelial cell permeability and membrane injury by targeting SERP1, which leads to dysfunction of endothelial cells and weakens vascular barrier function involved in the development of ALI. MiR-1-3p and SERP1 may be promising therapeutic candidates for sepsis-induced lung injury.

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Petsalaki, Eleni, Tonia Akoumianaki, Elizabeth J. Black, David A. F. Gillespie y George Zachos. "Phosphorylation at serine 331 is required for Aurora B activation". Journal of Cell Biology 195, n.º 3 (24 de octubre de 2011): 449–66. http://dx.doi.org/10.1083/jcb.201104023.

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Aurora B kinase activity is required for successful cell division. In this paper, we show that Aurora B is phosphorylated at serine 331 (Ser331) during mitosis and that phosphorylated Aurora B localizes to kinetochores in prometaphase cells. Chk1 kinase is essential for Ser331 phosphorylation during unperturbed prometaphase or during spindle disruption by taxol but not nocodazole. Phosphorylation at Ser331 is required for optimal phosphorylation of INCENP at TSS residues, for Survivin association with the chromosomal passenger complex, and for complete Aurora B activation, but it is dispensable for Aurora B localization to centromeres, for autophosphorylation at threonine 232, and for association with INCENP. Overexpression of Aurora BS331A, in which Ser331 is mutated to alanine, results in spontaneous chromosome missegregation, cell multinucleation, unstable binding of BubR1 to kinetochores, and impaired mitotic delay in the presence of taxol. We propose that Chk1 phosphorylates Aurora B at Ser331 to fully induce Aurora B kinase activity. These results indicate that phosphorylation at Ser331 is an essential mechanism for Aurora B activation.

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Shi, Yi, Ze Liu, Qian Zhang, Ingrid Vallee, Zhongying Mo, Shuji Kishi y Xiang-Lei Yang. "Phosphorylation of seryl-tRNA synthetase by ATM/ATR is essential for hypoxia-induced angiogenesis". PLOS Biology 18, n.º 12 (22 de diciembre de 2020): e3000991. http://dx.doi.org/10.1371/journal.pbio.3000991.

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Hypoxia-induced angiogenesis maintains tissue oxygen supply and protects against ischemia but also enhances tumor progression and malignancy. This is mediated through activation of transcription factors like hypoxia-inducible factor 1 (HIF-1) and c-Myc, yet the impact of hypoxia on negative regulators of angiogenesis is unknown. During vascular development, seryl-tRNA synthetase (SerRS) regulates angiogenesis through a novel mechanism by counteracting c-Myc and transcriptionally repressing vascular endothelial growth factor A (VEGFA) expression. Here, we reveal that the transcriptional repressor role of SerRS is inactivated under hypoxia through phosphorylation by ataxia telangiectasia mutated (ATM) and ataxia telangiectasia mutated and RAD3-related (ATR) at Ser101 and Ser241 to attenuate its DNA binding capacity. In zebrafish, SerRSS101D/S241D, a phosphorylation-mimicry mutant, cannot suppress VEGFA expression to support normal vascular development. Moreover, expression of SerRSS101A/S241A, a phosphorylation-deficient and constitutively active mutant, prevents hypoxia-induced binding of c-Myc and HIF-1 to the VEGFA promoter, and activation of VEGFA expression. Consistently, SerRSS101A/S241A strongly inhibits normal and tumor-derived angiogenesis in mice. Therefore, we reveal a key step regulating hypoxic angiogenesis and highlight the importance of nuclear SerRS in post-developmental angiogenesis regulation in addition to vascular development. The role of nuclear SerRS in inhibiting both c-Myc and HIF-1 may provide therapeutic opportunities to correct dysregulation of angiogenesis in pathological settings.

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Bernstein, Barton J. "Interpreting the Elusive Robert Serber: What Serber Says and What Serber Does Not Explicitly Say". Studies in History and Philosophy of Science Part B: Studies in History and Philosophy of Modern Physics 32, n.º 3 (septiembre de 2001): 443–86. http://dx.doi.org/10.1016/s1355-2198(01)00017-x.

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30

Schaafhausen, Anne, Simone Rost, Johannes Oldenburg y Clemens Müller. "Identification of VKORC1 interaction partners by split-ubiquitin system and coimmunoprecipitation". Thrombosis and Haemostasis 105, n.º 02 (2011): 285–94. http://dx.doi.org/10.1160/th10-07-0483.

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SummarySince the discovery of vitamin K epoxide reductase complex subunit 1 (VKORC1), the key enzyme for the regeneration of vitamin KH2, numerous studies have addressed the role of VKORC1 in the posttranslational modification of vitamin K-dependent proteins. VKORC1 is also the target protein of anticoagulant drugs of the coumarin type (e.g. warfarin). Genetic variants in VKORC1 have recently been shown to significantly affect the coumarin dose and international normalised ratio level. In the present study, we have used the split-ubiquitin yeast two-hybrid system to identify potential interaction partners of VKORC1. With this system we could identify 90 candidates. Out of these, we focused on VKORC1 itself, its paralog VKORC1L1, emopamil binding protein (EBP) and stress-associated endoplasmic reticulum protein 1 (SERP1). By coimmunprecipitation and colocalisation experiments, we were able to demonstrate evidence for the interaction of these proteins. Mutations in the EBP gene cause X-linked dominant chondrodysplasia punctata (CDPX2) which can be considered as a phenocopy of warfarin embryo-pathy. The interaction could be a link between these phenotypes. SERP1 represents an oxidative stress-associated endoplasmatic reticulum protein with chaperon-like functions. Antioxidant capacities have been described for vitamin K hydroquinone, the substrate of VKORC1. Both VKORC1 and SERP1, might have a synergistic function in eliminating reactive oxygen species generated during the VKOR redox process. Further studies are needed to investigate the role of these proteins in the vitamin K pathway.

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31

Vieweg, Sophie, Katie Mulholland, Bastian Bräuning, Nitin Kachariya, Yu-Chiang Lai, Rachel Toth, Pawan Kishor Singh et al. "PINK1-dependent phosphorylation of Serine111 within the SF3 motif of Rab GTPases impairs effector interactions and LRRK2-mediated phosphorylation at Threonine72". Biochemical Journal 477, n.º 9 (11 de mayo de 2020): 1651–68. http://dx.doi.org/10.1042/bcj20190664.

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Loss of function mutations in the PTEN-induced kinase 1 (PINK1) kinase are causal for autosomal recessive Parkinson's disease (PD) whilst gain of function mutations in the LRRK2 kinase cause autosomal dominant PD. PINK1 indirectly regulates the phosphorylation of a subset of Rab GTPases at a conserved Serine111 (Ser111) residue within the SF3 motif. Using genetic code expansion technologies, we have produced stoichiometric Ser111-phosphorylated Rab8A revealing impaired interactions with its cognate guanine nucleotide exchange factor and GTPase activating protein. In a screen for Rab8A kinases we identify TAK1 and MST3 kinases that can efficiently phosphorylate the Switch II residue Threonine72 (Thr72) in a similar manner as LRRK2 in vitro. Strikingly, we demonstrate that Ser111 phosphorylation negatively regulates the ability of LRRK2 but not MST3 or TAK1 to phosphorylate Thr72 of recombinant nucleotide-bound Rab8A in vitro and demonstrate an interplay of PINK1- and LRRK2-mediated phosphorylation of Rab8A in transfected HEK293 cells. Finally, we present the crystal structure of Ser111-phosphorylated Rab8A and nuclear magnetic resonance structure of Ser111-phosphorylated Rab1B. The structures reveal that the phosphorylated SF3 motif does not induce any major changes, but may interfere with effector-Switch II interactions through intramolecular H-bond formation and/or charge effects with Arg79. Overall, we demonstrate antagonistic regulation between PINK1-dependent Ser111 phosphorylation and LRRK2-mediated Thr72 phosphorylation of Rab8A indicating a potential cross-talk between PINK1-regulated mitochondrial homeostasis and LRRK2 signalling that requires further investigation in vivo.

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32

Zhang, Xiuyuan, Shan Gao, Jinfeng Niu, Pan Li, Juan Deng, Shixin Xu, Zhihong Wang, Weiwei Wang, Deling Kong y Chen Li. "Cannabinoid 2 Receptor Agonist Improves Systemic Sensitivity to Insulin in High-Fat Diet/Streptozotocin-Induced Diabetic Mice". Cellular Physiology and Biochemistry 40, n.º 5 (2016): 1175–85. http://dx.doi.org/10.1159/000453171.

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Background/Aims: The endocannabinoid signalling (ECS) system has been known to regulate glucose homeostasis. Previous studies have suggested that the cannabinoid 2 (CB2) receptor may play a regulatory role on insulin secretion, immune modulation and insulin resistance. Given that diabetes and insulin resistance are attributable to elevated inflammatory tone, we investigated the role of CB2 receptor on glucose tolerance and insulin sensitivity in high-fat diet (HFD)/streptozotocin (STZ)-induced mice. Methods: Diabetes was induced in male ICR mice by HFD/STZ and exposed to a CB2 receptor agonist, SER601, for 2- or 4-weeks via subcutaneous implantation of osmotic minipumps. Glucose and insulin tolerance tests were performed at the end of treatment. Islets were isolated for assessment of β-cell function. Pancreases and skeletal muscles were also obtained for histological analyses. Results: Despite a lack of impact on glucose tolerance, substantial improvement on insulin sensitivity was observed in SER601-treated mice, which could partly be attributed to improved islet β-cell function, shown as increased glucose-induced insulin secretion and insulin content. No changes on islet macrophage infiltration or skeletal muscle fat deposition were detectable from SER601-treated mice. However, a major decrease in body weight was recorded at the end of 4-week SER601 exposure, accompanied by a lack of epididymal adipose mass in SER601-treated mice. Conclusion: Our data suggest a lipolytic role of SER601 in HFD/STZ-induced diabetic mice, which results in significant improvement of systemic insulin sensitivity. Thus, the CB2 receptor may be considered a promising target for therapeutic development against insulin resistance and obesity-related diabetes.

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33

Hornby, Richard. "Serban vs. Schreiber". Hudson Review 53, n.º 1 (2000): 92. http://dx.doi.org/10.2307/3853104.

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SERBAN, GEORGE. "Dr. Serban Replies". American Journal of Psychiatry 142, n.º 5 (mayo de 1985): 665—a—666. http://dx.doi.org/10.1176/ajp.142.5.665-a.

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35

Santana, Juan Carlos. "The Serape Effect". Strength and Conditioning Journal 25, n.º 2 (abril de 2003): 73–74. http://dx.doi.org/10.1519/00126548-200304000-00013.

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36

Gordeuk, Victor R., Xu Zhang, Wei Zhang, Shwu-Fan Ma, Galina Miasniakova, Adelina Sergueeva, Tatiana Ammosova et al. "Iron Deficiency Modifies Gene Expression Variation Induced by Augmented Hypoxia Sensing". Blood 120, n.º 21 (16 de noviembre de 2012): 1765. http://dx.doi.org/10.1182/blood.v120.21.1765.1765.

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Abstract Abstract 1765 Hypoxia may cause pulmonary and brain edema, pulmonary hypertension, aberrant metabolism and early mortality. To better understand pathological processes associated with hypoxia, we examined gene expression in Chuvash polycythemia blood mononuclear cells. Chuvash polycythemia is a congenital disorder of up-regulated hypoxic response at normoxia wherein VHLR200W homozygosity leads to elevated hypoxia inducible factor (HIF)-1 and HIF-2 levels, thromboses, pulmonary hypertension, lower systemic blood pressure (SBP) and increased mortality. VHLR200W homozygotes are often treated by phlebotomy resulting in iron deficiency, allowing us to evaluate an interaction of augmented hypoxia sensing with iron deficiency. Expression profiling of 8 VHLR200W homozygotes and 17 VHL wildtype individuals, matched for normal iron status as reflected in serum ferritin concentration, revealed altered regulation of 3069 genes at false discovery rate <0.05, with 847 up-regulated and 2222 down-regulated in VHLR200W homozygotes. Genes induced by homozygous VHLR200W were enriched in immune response pathways; those repressed in RNA transcription and protein synthesis pathways. Forty-two genes showed a >1.5-fold change in expression level, mostly (74%) an increase. Seven showed a >2-fold increase: CA1 (carbonic anhydrase), SELENBP1 (selenium binding protein 1), IL1B (interleukin 1 beta), SLC4A1 (solute carrier family 4 member 1), HBB (hemoglobin beta), and AHSP (alpha hemoglobin stabilizing protein). Additional studies including 16 VHLR200W homozygotes with low ferritin indicated that iron deficiency enhanced the induction effect of VHLR200W for 51 of the 847 upregulated genes and suppressed the induction effect for 108 of the upregulated genes. Genes further upregulated by iron deficiency included CA1, CSDA (cold shock domain protein A), BCL2L1 (BCL-2 like 1), BPGM (2,3-bisphosphoglycerate mutase), DCAF12 (DDB1 and CUL4 associated factor 12), FECH (ferrochelatase), SELENBP1 and SLC4A1. Genes for which iron deficiency suppressed the induction included inflammatory and immune pathway genes such as CASP5, CXCL16, IFI30, IFI35, IRF5, LILRB1, NOD2, RELT, TCIRG1 and TNFAIP2. A number of the genes with altered regulation in VHLR200W homozygotes might modify risk of thrombosis (upregulated: F3, SERPINE1, SERPINB2, SERPING1, PLAUR, THBD; down regulated: SERBP1), elevated systolic pulmonary artery pressure (upregulated: HTR1B, THBS1; downregulated: S1PR1, STIM2), or benign hemangioma (downregulated: CCM2). However, expression of these genes tended not to be influenced by iron status. VEGF was induced in VHLR200W homozygotes and surprisingly this induction was suppressed by iron deficiency. Expression relationships suggested a broad effect of VHLR200W in reducing systolic blood pressure through inducing VEGF. We demonstrate that many genes have commensurate changes of their expression by both iron deficiency and VHLR200W associated normoxic up-regulation of HIFs, as expected. However, there are genes that are regulated asynchronously. Further research is needed to define the molecular bases of separate regulation of genes by HIFs and iron status and to define relative risks and benefits of therapeutic phlebotomy for polycythemia. The resulting elucidation of the genomic pathways affecting predisposition to thromboses, pulmonary hypertension, lower systolic blood pressure and the interaction of augmented hypoxia sensing with iron deficiency should have broad implications leading to a better understanding of the pathophysiology of many diseases and the development of targeted therapies. Disclosures: No relevant conflicts of interest to declare.

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Relic, Biserka, Celine Deroyer, Olivier Malaise, Zelda Plener, Philippe Gillet, Dominique de Seny y Michel G. Malaise. "TFEB phosphorylation on Serine 211 is induced by autophagy in human synovial fibroblasts and by p62/SQSTM1 overexpression in HEK293 cells". Biochemical Journal 478, n.º 16 (27 de agosto de 2021): 3145–55. http://dx.doi.org/10.1042/bcj20210174.

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Autophagy receptor p62/SQSTM1 signals a complex network that links autophagy-lysosomal system to proteasome. Phosphorylation of p62 on Serine 349 (P-Ser349 p62) is involved in a cell protective, antioxidant pathway. We have shown previously that P-Ser349 p62 occurs and is rapidly degraded during human synovial fibroblasts autophagy. In this work we observed that fingolimod (FTY720), used as a medication for multiple sclerosis, induced coordinated expression of p62, P-Ser349 p62 and inhibitory TFEB form, phosphorylated on Serine 211 (P-Ser211 TFEB), in human synovial fibroblasts. These effects were mimicked and potentiated by proteasome inhibitor MG132. In addition, FTY720 induced autophagic flux, LC3B-II up-regulation, Akt phosphorylation inhibition on Serine 473 but down-regulated TFEB, suggesting stalled autophagy. FTY720 decreased cytoplasmic fraction contained TFEB but induced TFEB in nuclear fraction. FTY720-induced P-Ser211 TFEB was mainly found in membrane fraction. Autophagy and VPS34 kinase inhibitor, autophinib, further increased FTY720-induced P-Ser349 p62 but inhibited concomitant expression of P-Ser211 TFEB. These results suggested that P-Ser211 TFEB expression depends on autophagy. Overexpression of GFP tagged TFEB in HEK293 cells showed concomitant expression of its phosphorylated form on Serine 211, that was down-regulated by autophinib. These results suggested that autophagy might be autoregulated through P-Ser211 TFEB as a negative feedback loop. Of interest, overexpression of p62, p62 phosphorylation mimetic (S349E) mutant and phosphorylation deficient mutant (S349A) in HEK293 cells markedly induced P-Ser211 TFEB. These results showed that p62 is involved in regulation of TFEB phosphorylation on Serine 211 but that this involvement does not depend on p62 phosphorylation on Serine 349.

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38

Vichaiwong, Kanokwan, Suneet Purohit, Ding An, Taro Toyoda, Niels Jessen, Michael F. Hirshman y Laurie J. Goodyear. "Contraction regulates site-specific phosphorylation of TBC1D1 in skeletal muscle". Biochemical Journal 431, n.º 2 (28 de septiembre de 2010): 311–20. http://dx.doi.org/10.1042/bj20101100.

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TBC1D1 (tre-2/USP6, BUB2, cdc16 domain family member 1) is a Rab-GAP (GTPase-activating protein) that is highly expressed in skeletal muscle, but little is known about TBC1D1 regulation and function. We studied TBC1D1 phosphorylation on three predicted AMPK (AMP-activated protein kinase) phosphorylation sites (Ser231, Ser660 and Ser700) and one predicted Akt phosphorylation site (Thr590) in control mice, AMPKα2 inactive transgenic mice (AMPKα2i TG) and Akt2-knockout mice (Akt2 KO). Muscle contraction significantly increased TBC1D1 phosphorylation on Ser231 and Ser660, tended to increase Ser700 phosphorylation, but had no effect on Thr590. AICAR (5-aminoimidazole-4-carboxyamide ribonucleoside) also increased phosphorylation on Ser231, Ser660 and Ser700, but not Thr590, whereas insulin only increased Thr590 phosphorylation. Basal and contraction-stimulated TBC1D1 Ser231, Ser660 and Ser700 phosphorylation were greatly reduced in AMPKα2i TG mice, although contraction still elicited a small increase in phosphorylation. Akt2 KO mice had blunted insulin-stimulated TBC1D1 Thr590 phosphorylation. Contraction-stimulated TBC1D1 Ser231 and Ser660 phosphorylation were normal in high-fat-fed mice. Glucose uptake in vivo was significantly decreased in tibialis anterior muscles overexpressing TBC1D1 mutated on four predicted AMPK phosphorylation sites. In conclusion, contraction causes site-specific phosphorylation of TBC1D1 in skeletal muscle, and TBC1D1 phosphorylation on AMPK sites regulates contraction-stimulated glucose uptake. AMPK and Akt regulate TBC1D1 phosphorylation, but there must be additional upstream kinases that mediate TBC1D1 phosphorylation in skeletal muscle.

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39

Nomura, Atsuo, Shunichi Yokoe, Kiichiro Tomoda, Takatoshi Nakagawa, Francisco Javier Martin-Romero y Michio Asahi. "Fluctuation in O-GlcNAcylation inactivates STIM1 to reduce store-operated calcium ion entry via down-regulation of Ser621 phosphorylation". Journal of Biological Chemistry 295, n.º 50 (6 de octubre de 2020): 17071–82. http://dx.doi.org/10.1074/jbc.ra120.014271.

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Stromal interaction molecule 1 (STIM1) plays a pivotal role in store-operated Ca2+ entry (SOCE), an essential mechanism in cellular calcium signaling and in maintaining cellular calcium balance. Because O-GlcNAcylation plays pivotal roles in various cellular function, we examined the effect of fluctuation in STIM1 O-GlcNAcylation on SOCE activity. We found that both increase and decrease in STIM1 O-GlcNAcylation impaired SOCE activity. To determine the molecular basis, we established STIM1-knockout HEK293 (STIM1-KO-HEK) cells using the CRISPR/Cas9 system and transfected STIM1 WT (STIM1-KO-WT-HEK), S621A (STIM1-KO-S621A-HEK), or T626A (STIM1-KO-T626A-HEK) cells. Using these cells, we examined the possible O-GlcNAcylation sites of STIM1 to determine whether the sites were O-GlcNAcylated. Co-immunoprecipitation analysis revealed that Ser621 and Thr626 were O-GlcNAcylated and that Thr626 was O-GlcNAcylated in the steady state but Ser621 was not. The SOCE activity in STIM1-KO-S621A-HEK and STIM1-KO-T626A-HEK cells was lower than that in STIM1-KO-WT-HEK cells because of reduced phosphorylation at Ser621. Treatment with the O-GlcNAcase inhibitor Thiamet G or O-GlcNAc transferase (OGT) transfection, which increases O-GlcNAcylation, reduced SOCE activity, whereas treatment with the OGT inhibitor ST045849 or siOGT transfection, which decreases O-GlcNAcylation, also reduced SOCE activity. Decrease in SOCE activity due to increase and decrease in O-GlcNAcylation was attributable to reduced phosphorylation at Ser621. These data suggest that both decrease in O-GlcNAcylation at Thr626 and increase in O-GlcNAcylation at Ser621 in STIM1 lead to impairment of SOCE activity through decrease in Ser621 phosphorylation. Targeting STIM1 O-GlcNAcylation could provide a promising treatment option for the related diseases, such as neurodegenerative diseases.

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40

Gaffney, Kristen A. y Heedeok Hong. "The rhomboid protease GlpG has weak interaction energies in its active site hydrogen bond network". Journal of General Physiology 151, n.º 3 (12 de noviembre de 2018): 282–91. http://dx.doi.org/10.1085/jgp.201812047.

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Intramembrane rhomboid proteases are of particular interest because of their function to hydrolyze a peptide bond of a substrate buried in the membrane. Crystal structures of the bacterial rhomboid protease GlpG have revealed a catalytic dyad (Ser201-His254) and oxyanion hole (His150/Asn154/the backbone amide of Ser201) surrounded by the protein matrix and contacting a narrow water channel. Although multiple crystal structures have been solved, the catalytic mechanism of GlpG is not completely understood. Because it is a serine protease, hydrogen bonding interactions between the active site residues are thought to play a critical role in the catalytic cycle. Here, we dissect the interaction energies among the active site residues His254, Ser201, and Asn154 of Escherichia coli GlpG, which form a hydrogen bonding network. We combine double mutant cycle analysis with stability measurements using steric trapping. In mild detergent, the active site residues are weakly coupled with interaction energies (ΔΔGInter) of ‒1.4 kcal/mol between His254 and Ser201 and ‒0.2 kcal/mol between Ser201 and Asn154. Further, by analyzing the propagation of single mutations of the active site residues, we find that these residues are important not only for function but also for the folding cooperativity of GlpG. The weak interaction between Ser and His in the catalytic dyad may partly explain the unusually slow proteolysis by GlpG compared with other canonical serine proteases. Our result suggests that the weak hydrogen bonds in the active site are sufficient to carry out the proteolytic function of rhomboid proteases.

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41

Pais, A. "Robert Serber (1909 – 1997)". Physics in Perspective 1, n.º 1 (marzo de 1999): 105–9. http://dx.doi.org/10.1007/s000160050008.

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Santana, Juan C., Stuart M. McGill y Lee E. Brown. "Anterior and Posterior Serape". Strength and Conditioning Journal 37, n.º 5 (octubre de 2015): 8–13. http://dx.doi.org/10.1519/ssc.0000000000000162.

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43

Jennifer Borges Foster. "from "Seraph"". Prairie Schooner 83, n.º 1 (2009): 63–64. http://dx.doi.org/10.1353/psg.0.0189.

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Uebi, Tatsuya, Mitsuhiro Tamura, Nanao Horike, Yoshiko Katoh Hashimoto y Hiroshi Takemori. "Phosphorylation of the CREB-specific coactivator TORC2 at Ser307 regulates its intracellular localization in COS-7 cells and in the mouse liver". American Journal of Physiology-Endocrinology and Metabolism 299, n.º 3 (septiembre de 2010): E413—E425. http://dx.doi.org/10.1152/ajpendo.00525.2009.

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The CREB-specific coactivator TORC2 (also known as CRTC2) upregulates gluconeogenic gene expression in the liver. Salt-inducible kinase (SIK) family enzymes inactivate TORC2 through phosphorylation and localize it in the cytoplasm. Ser171 and Ser275 were found to be phosphorylated in pancreatic β-cells. Calcineurin (Cn) is proposed as the Ser275 phosphatase, because its inhibitor cyclosporin A (CsA) stabilizes phospho-Ser275 and retains TORC2 in the cytoplasm. Because the regulation of dephosphorylation at Ser171 has not been fully clarified, we performed experiments with a range of doses of okadaic acid (OA), an inhibitor of PP2A/PP1, and with overexpression of various phosphatases and found that PP1 functions as an activator for TORC2, whereas PP2A acts as an inhibitor. In further studies using TORC2 mutants, we detected a disassociation between the intracellular distribution and the transcription activity of TORC2. Additional mutant analyses suggested the presence of a third phosphorylation site, Ser307. The Ser307-disrupted TORC2 was constitutively localized in the nucleus, but its coactivator activity was normally suppressed by SIK1 in COS-7 cells. CsA, but not OA, stabilized the phosphogroup at Ser307, suggesting that differential dephosphorylation at Ser171 and Ser307 cooperatively regulate TORC2 activity and that the nuclear localization of TORC2 is insufficient to function as a coactivator. Because the COS-7 cell line may not possess signaling cascades for gluconeogenic programs, we next examined the importance of Ser307 and Ser171 for TORC2's function in mouse liver. Levels of phosphorylation at Ser171 and Ser307 changed in response to fasting or fed conditions and insulin resistance of the mouse liver, which were modified by treatment with CsA/OA and by overexpression of PP1/PP2A/Cn. These results suggest that multiple phosphorylation sites and their phosphatases may play important roles in regulating TORC2/CREB-mediated gluconeogenic programs in the liver.

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45

Christensen, Brian, Mette S. Nielsen, Kim F. Haselmann, Torben E. Petersen y Esben S. Sørensen. "Post-translationally modified residues of native human osteopontin are located in clusters: identification of 36 phosphorylation and five O-glycosylation sites and their biological implications". Biochemical Journal 390, n.º 1 (9 de agosto de 2005): 285–92. http://dx.doi.org/10.1042/bj20050341.

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OPN (osteopontin) is an integrin-binding highly phosphorylated glycoprotein, recognized as a key molecule in a multitude of biological processes such as bone mineralization, cancer metastasis, cell-mediated immune response, inflammation and cell survival. A significant regulation of OPN function is mediated through PTM (post-translational modification). Using a combination of Edman degradation and MS analyses, we have characterized the complete phosphorylation and glycosylation pattern of native human OPN. A total of 36 phosphoresidues have been localized in the sequence of OPN. There are 29 phosphorylations (Ser8, Ser10, Ser11, Ser46, Ser47, Thr50, Ser60, Ser62, Ser65, Ser83, Ser86, Ser89, Ser92, Ser104, Ser110, Ser113, Thr169, Ser179, Ser208, Ser218, Ser238, Ser247, Ser254, Ser259, Ser264, Ser275, Ser287, Ser292 and Ser294) located in the target sequence of MGCK (mammary gland casein kinase) also known as the Golgi kinase (S/T-X-E/S(P)/D). Six phosphorylations (Ser101, Ser107, Ser175, Ser199, Ser212 and Ser251) are located in the target sequence of CKII (casein kinase II) [S-X-X-E/S(P)/D] and a single phosphorylation, Ser203, is not positioned in the motif of either MGCK or CKII. The 36 phosphoresidues represent the maximal degree of modification since variability at many sites was seen. Five threonine residues are O-glycosylated (Thr118, Thr122, Thr127, Thr131 and Thr136) and two potential sites for N-glycosylation (Asn63 and Asn90) are not occupied in human milk OPN. The phosphorylations are arranged in clusters of three to five phosphoresidues and the regions containing the glycosylations and the RGD (Arg-Gly-Asp) integrin-binding sequence are devoid of phosphorylations. Knowledge about the positions and nature of PTMs in OPN will allow a rational experimental design of functional studies aimed at understanding the structural and functional interdependences in diverse biological processes in which OPN is a key molecule.

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Vázquez, Patricia, Isabel Roncero, Enrique Blázquez y Elvira Alvarez. "Substitution of the cysteine 438 residue in the cytoplasmic tail of the glucagon-like peptide-1 receptor alters signal transduction activity". Journal of Endocrinology 185, n.º 1 (abril de 2005): 35–44. http://dx.doi.org/10.1677/joe.1.06031.

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Several G-protein-coupled receptors contain cysteine residues in the C-terminal tail that may modulate receptor function. In this work we analysed the substitution of Cys438 by alanine in the glucagon-like peptide-1 (GLP-1) receptor (GLPR), which led to a threefold decrease in cAMP production, although endocytosis and cellular redistribution of GLP-1 receptor agonist-induced processes were unaffected. Additionally, cysteine residues in the C-terminal tail of several G-protein-coupled receptors were found to act as substrates for palmitoylation, which might modify the access of protein kinases to this region. His-tagged GLP-1 receptors incorporated 3H-palmitate. Nevertheless, substitution of Cys438 prevented the incorporation of palmitate. Accordingly, we also investigated the effect of substitution of the consensus sequence by protein kinase C (PKC) Ser431/432 in both wild-type and Ala438 GLP-1 receptors. Substitution of Ser431/432 by alanine did not modify the ability of wild-type receptors to stimulate adenylate cyclase or endocytosis and recycling processes. By contrast, the substitution of Ser431/432 by alanine in the receptor containing Ala438 increased the ability to stimulate adenylate cyclase. All types of receptors were mainly internalised through coated pits. Thus, cysteine 438 in the cytoplasmic tail of the GLP-1 receptor would regulate its interaction with G-proteins and the stimulation of adenylyl cyclase. Palmitoylation of this residue might control the access of PKC to Ser431/432.

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Mansuri, Mohmmad Shoab, Mala Singh y Shahnawaz D. Jadeja. "An in Vitro Study Elucidating the Effect of Oxidative Stress on Melanocytes". International Journal of Research and Review 8, n.º 2 (26 de mayo de 2021): 142–54. http://dx.doi.org/10.52403/ijrr.20210222.

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Oxidative stress plays a major role in melanocyte destruction in vitiligo, however the exact mechanism responsible for melanocyte death remains uncertain. We aimed to examine the effect of oxidative stress on melanocyte viability by MTT assay and expression of antioxidant genes (CAT, GPX1, G6PD and PRDX3), stress related genes (HSP60, HSP70, SERP1, SIRT1 and POLH) and melanocyte specific genes (MITF, TYR, TYRP1, TRPM1, EDN1, EZR and LAMP1) by real-time PCR upon exposing the normal human melanocytes (NHM), immortalized melanocytes derived from healthy human (PIG1) and from vitiligo patient (PIG3V) to cumene hydroperoxide (CHP). The transcript levels of selected genes were estimated by using real-time PCR. The NHM, PIG1 and PIG3V melanocytes showed significant decrease in viability under CHP (10-100μM) induced oxidative stress. PIG3V displayed significantly increased expression of PRDX3, HSP70, SERP1, POLH as well as decreased expression of CAT, MITF, TYR, TYRP1, TRPM1, EDN1 and LAMP1 under CHP (10 & 20μM) treatment, as compared to NHM and/or PIG1 melanocytes. These results suggest that vitiligo melanocytes are more sensitive to CHP induced oxidative stress, as compared to normal melanocytes. The present study demonstrates that vitiligo may result from an insufficient response of melanocytes to oxidative stress induced by high H2O2 levels. Keywords: Vitiligo; melanocyte; PIG1; PIG3V; oxidative stress; cumene hydroperoxide (CHP).

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Stegert, Mario R., Alexander Hergovich, Rastislav Tamaskovic, Samuel J. Bichsel y Brian A. Hemmings. "Regulation of NDR Protein Kinase by Hydrophobic Motif Phosphorylation Mediated by the Mammalian Ste20-Like Kinase MST3". Molecular and Cellular Biology 25, n.º 24 (15 de diciembre de 2005): 11019–29. http://dx.doi.org/10.1128/mcb.25.24.11019-11029.2005.

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ABSTRACT NDR protein kinases are involved in the regulation of cell cycle progression and morphology. NDR1/NDR2 protein kinase is activated by phosphorylation on the activation loop phosphorylation site Ser281/Ser282 and the hydrophobic motif phosphorylation site Thr444/Thr442. Autophosphorylation of NDR is responsible for phosphorylation on Ser281/Ser282, whereas Thr444/Thr442 is targeted by an upstream kinase. Here we show that MST3, a mammalian Ste20-like protein kinase, is able to phosphorylate NDR protein kinase at Thr444/Thr442. In vitro, MST3 selectively phosphorylated Thr442 of NDR2, resulting in a 10-fold stimulation of NDR activity. MOB1A (Mps one binder 1A) protein further increased the activity, leading to a fully active kinase. In vivo, Thr442 phosphorylation after okadaic acid stimulation was potently inhibited by MST3KR, a kinase-dead mutant of MST3. Knockdown of MST3 using short hairpin constructs abolished Thr442 hydrophobic motif phosphorylation of NDR in HEK293F cells. We conclude that activation of NDR is a multistep process involving phosphorylation of the hydrophobic motif site Thr444/2 by MST3, autophosphorylation of Ser281/2, and binding of MOB1A.

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Nedeljković, Sasa. "Rahvus kui religioosne kategooria, natsionalism kui ontoloogia. Serbia juhtum". Mäetagused 26 (2004): 9–22. http://dx.doi.org/10.7592/mt2004.26.serbia.

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Serber, Zach. "A Conversation with Zach Serber". Industrial Biotechnology 15, n.º 6 (1 de diciembre de 2019): 325–27. http://dx.doi.org/10.1089/ind.2019.29193.zse.

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