Journal articles: 'Regulation scaffolding'

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Alderton, Gemma K. "Scaffolding the regulation of hypoxia." Nature Reviews Cancer 12, no. 3 (February 24, 2012): 153. http://dx.doi.org/10.1038/nrc3242.

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Myruski, Sarah, Samantha Birk, Mayumi Karasawa, Aya Kamikubo, Midori Kazama, Hidemi Hirabayashi, and Tracy Dennis-Tiwary. "Neural signatures of child cognitive emotion regulation are bolstered by parental social regulation in two cultures." Social Cognitive and Affective Neuroscience 14, no. 9 (September 2019): 947–56. http://dx.doi.org/10.1093/scan/nsz070.

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Abstract Caregiver impact on the efficacy of cognitive emotion regulation (ER; i.e. reappraisal) during childhood is poorly understood, particularly across cultures. We tested the hypothesis that in children from Japan and the USA, a neurocognitive signature of effective reappraisal, the late positive potential (LPP), will be bolstered by cognitive scaffolding by parents, and explored whether the two cultures differed in whether mere physical proximity of parents provides similar benefit. Five-to-seven-year-olds (N = 116; nJapan = 58; nUSA = 58) completed a directed reappraisal task (EEG-recorded) in one of three contexts: (i) parent-scaffolding, (ii) parent-present and (iii) parent-absent. Across cultures, those in the parent-scaffolding group and parent-present group showed effective reappraisal via the LPP relative to those in the parent-absent group. Results suggest that scaffolding is an effective method through which parents in these two cultures buttress child ER, and even parental passive proximity appears to have a meaningful effect on child ER across cultures.

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Umar, Tariq, Nnedinma Umeokafor, Mohamed Shaik Honnur Vali, and Asad Zia. "A Comparative Study of Occupational Safety and Health (OS&H) Regulations in United States, United Kingdom, Australia, South Africa, and Oman." IOP Conference Series: Earth and Environmental Science 1101, no. 3 (November 1, 2022): 032016. http://dx.doi.org/10.1088/1755-1315/1101/3/032016.

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Abstract This article identifies the gaps in OS&H regulations in Omani construction using a critical review and analysis of relevant literature. Four countries United States of America (USA), United Kingdom (UK), Australia (AUS), and South Africa (SA) were then compared to Oman in relation to selected regulations. The study reveals fall from a height is one of the main causes of accidents in different sectors in Oman however there are no specific regulations that cover this cause of accidents in detail. The only regulation which applies to the “fall from a height” is the regulation of OS&H, issued by the Ministry of Manpower. Overall, the whole regulations applicable in Oman shows that although the term fall, appear several times in the regulation, the full spectrum of the fall protection is not covered in detail. The provision of chemical hazards in Omani regulations is not of the standards as adopted in the USA, UK, AUS, and SA. There is limited information for the regulated to support adequate compliance. While the term “scaffolding” was not found in the current regulations enforced in Oman, the term “ladder” was, however, used at five different instances in the regulations which obviously cannot substitute the scaffolding.

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Mauban, J. R. H., M. O’Donnell, S. Warrier, S. Manni, and M. Bond. "AKAP-Scaffolding Proteins and Regulation of Cardiac Physiology." Physiology 24, no. 2 (April 2009): 78–87. http://dx.doi.org/10.1152/physiol.00041.2008.

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A kinase anchoring proteins (AKAPs) compose a growing list of diverse but functionally related proteins defined by their ability to bind to the regulatory subunit of protein kinase A. AKAPs perform an integral role in the spatiotemporal modulation of a multitude of cellular signaling pathways. This review highlights the extensive role of AKAPs in cardiac excitation/contraction coupling and cardiac physiology. The literature shows that particular AKAPs are involved in cardiac Ca2+ influx, release, reuptake, and myocyte repolarization. Studies have also suggested roles for AKAPs in cardiac remodeling. Transgenic studies show functional effects of AKAPs, not only in the cardiovascular system but in other organ systems as well.

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He, Dao-Yao, Jérémie Neasta, and Dorit Ron. "Epigenetic Regulation ofBDNFExpression via the Scaffolding Protein RACK1." Journal of Biological Chemistry 285, no. 25 (April 21, 2010): 19043–50. http://dx.doi.org/10.1074/jbc.m110.100693.

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Ferreira, Marília Mendes. "Constraints to peer scaffolding." Trabalhos em Linguística Aplicada 47, no. 1 (June 2008): 9–29. http://dx.doi.org/10.1590/s0103-18132008000100002.

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Several studies, usually carried out in settings that are conducive to interaction, demonstrate peers can provide mutual scaffolding effectively. In contrast, this article focuses on constraints to peer scaffolding which, possibly, happened because of participants' demotivating learning environment. Analysis is based on the video and audio recordings of the performance of two beginning Brazilian students carrying out two oral tasks in an EFL class. Task one consists of an information gap and task two, of a communicative drill. The following constraints were identified: 1) the less capable peer's object-regulation, 2) the more capable peer's hindrance to scaffolding, 3) the more capable peer's lack of L2 knowledge. These hindrances can be explained by the students' pervasive and frustrating foreign language learning experience in the Brazilian public school and by the lack of socialization into scaffolding.

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Augustin, Vanessa, and Stefan Kins. "Fe65: A Scaffolding Protein of Actin Regulators." Cells 10, no. 7 (June 25, 2021): 1599. http://dx.doi.org/10.3390/cells10071599.

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The scaffolding protein family Fe65, composed of Fe65, Fe65L1, and Fe65L2, was identified as an interaction partner of the amyloid precursor protein (APP), which plays a key function in Alzheimer’s disease. All three Fe65 family members possess three highly conserved interaction domains, forming complexes with diverse binding partners that can be assigned to different cellular functions, such as transactivation of genes in the nucleus, modulation of calcium homeostasis and lipid metabolism, and regulation of the actin cytoskeleton. In this article, we rule out putative new intracellular signaling mechanisms of the APP-interacting protein Fe65 in the regulation of actin cytoskeleton dynamics in the context of various neuronal functions, such as cell migration, neurite outgrowth, and synaptic plasticity.

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Tyagarajan, Shiva K., Himanish Ghosh, Gonzalo E. Yévenes, Irina Nikonenko, Claire Ebeling, Cornelia Schwerdel, Corinne Sidler, et al. "Regulation of GABAergic synapse formation and plasticity by GSK3β-dependent phosphorylation of gephyrin." Proceedings of the National Academy of Sciences 108, no. 1 (December 20, 2010): 379–84. http://dx.doi.org/10.1073/pnas.1011824108.

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Postsynaptic scaffolding proteins ensure efficient neurotransmission by anchoring receptors and signaling molecules in synapse-specific subcellular domains. In turn, posttranslational modifications of scaffolding proteins contribute to synaptic plasticity by remodeling the postsynaptic apparatus. Though these mechanisms are operant in glutamatergic synapses, little is known about regulation of GABAergic synapses, which mediate inhibitory transmission in the CNS. Here, we focused on gephyrin, the main scaffolding protein of GABAergic synapses. We identify a unique phosphorylation site in gephyrin, Ser270, targeted by glycogen synthase kinase 3β (GSK3β) to modulate GABAergic transmission. Abolishing Ser270 phosphorylation increased the density of gephyrin clusters and the frequency of miniature GABAergic postsynaptic currents in cultured hippocampal neurons. Enhanced, phosphorylation-dependent gephyrin clustering was also induced in vitro and in vivo with lithium chloride. Lithium is a GSK3β inhibitor used therapeutically as mood-stabilizing drug, which underscores the relevance of this posttranslational modification for synaptic plasticity. Conversely, we show that gephyrin availability for postsynaptic clustering is limited by Ca2+-dependent gephyrin cleavage by the cysteine protease calpain-1. Together, these findings identify gephyrin as synaptogenic molecule regulating GABAergic synaptic plasticity, likely contributing to the therapeutic action of lithium.

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Okada, Yasunobu. "A scaffolding for regulation of volume-sensitive Cl−channels." Journal of Physiology 520, no. 1 (October 1999): 2. http://dx.doi.org/10.1111/j.1469-7793.1999.00002.x.

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Kim, Kiae, Yeonjin Han, Longhan Duan, and Ka Young Chung. "Scaffolding of Mitogen-Activated Protein Kinase Signaling by β-Arrestins." International Journal of Molecular Sciences 23, no. 2 (January 17, 2022): 1000. http://dx.doi.org/10.3390/ijms23021000.

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β-arrestins were initially identified to desensitize and internalize G-protein-coupled receptors (GPCRs). Receptor-bound β-arrestins also initiate a second wave of signaling by scaffolding mitogen-activated protein kinase (MAPK) signaling components, MAPK kinase kinase, MAPK kinase, and MAPK. In particular, β-arrestins facilitate ERK1/2 or JNK3 activation by scaffolding signal cascade components such as ERK1/2-MEK1-cRaf or JNK3-MKK4/7-ASK1. Understanding the precise molecular and structural mechanisms of β-arrestin-mediated MAPK scaffolding assembly would deepen our understanding of GPCR-mediated MAPK activation and provide clues for the selective regulation of the MAPK signaling cascade for therapeutic purposes. Over the last decade, numerous research groups have attempted to understand the molecular and structural mechanisms of β-arrestin-mediated MAPK scaffolding assembly. Although not providing the complete mechanism, these efforts suggest potential binding interfaces between β-arrestins and MAPK signaling components and the mechanism for MAPK signal amplification by β-arrestin-mediated scaffolding. This review summarizes recent developments of cellular and molecular works on the scaffolding mechanism of β-arrestin for MAPK signaling cascade.

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Calabrese, Barbara, Margaret S. Wilson, and Shelley Halpain. "Development and Regulation of Dendritic Spine Synapses." Physiology 21, no. 1 (February 2006): 38–47. http://dx.doi.org/10.1152/physiol.00042.2005.

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Dendritic spines are small protrusions from neuronal dendrites that form the postsynaptic component of most excitatory synapses in the brain. They play critical roles in synaptic transmission and plasticity. Recent advances in imaging and molecular technologies reveal that spines are complex, dynamic structures that contain a dense array of cytoskeletal, transmembrane, and scaffolding molecules. Several neurological and psychiatric disorders exhibit dendritic spine abnormalities.

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Redden, John M., Andrew V. Le, Arpita Singh, Kyle Federkiewicz, Samantha Smith, and Kimberly L. Dodge-Kafka. "Spatiotemporal regulation of PKC via interactions with AKAP7 isoforms." Biochemical Journal 446, no. 2 (August 14, 2012): 301–9. http://dx.doi.org/10.1042/bj20120366.

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The regulation of kinases by scaffolding proteins greatly contributes to the fidelity of signal transduction. In the present study, we explored an interaction between the ubiquitous enzyme PKC (protein kinase C) and the scaffolding protein AKAP7 (A-kinase-anchoring protein 7). Using protein biochemistry and surface plasmon resonance approaches, we demonstrate that both AKAP7γ and AKAP7α are capable of high-affinity interactions with multiple isoenzymes of PKC. Furthermore, this interaction is achieved via multi-site binding on both proteins. FRET (fluorescence resonance energy transfer) analysis using a PKC activity reporter suggests that anchoring of the kinase within AKAP7 complexes enhances the phosphorylation of substrate proteins. Finally, we determined using FRAP (fluorescence recovery after photobleaching) and virtual modelling that AKAP7 restricts the mobility of PKC within cells by tethering it to subcellular compartments. Collectively, the results of the present study suggests that AKAP7 could play an integral role in dictating PKC localization and function in tissues where the two proteins are co-expressed.

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Tyan, Leonid, Daniel Turner, Karlie R. Komp, Roman Y. Medvedev, Evi Lim, and Alexey V. Glukhov. "Caveolin-3 is required for regulation of transient outward potassium current by angiotensin II in mouse atrial myocytes." American Journal of Physiology-Heart and Circulatory Physiology 320, no. 2 (February 1, 2021): H787—H797. http://dx.doi.org/10.1152/ajpheart.00569.2020.

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Angiotensin II receptor 1 is associated with caveolae and caveolar scaffolding protein caveolin-3 in mouse atrial myocytes that is required for the regulation of Ito by angiotensin II. Downregulation of caveolae/caveolin-3 disrupts this regulation and may be implicated in pathophysiological atrial remodeling.

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Liebmann, Thomas, Nicolas Fritz, Markus Kruusmägi, Linda Westin, Kristoffer Bernhem, Alexander Bondar, Anita Aperia, and Hjalmar Brismar. "Regulation of Neuronal Na,K-ATPase by Extracellular Scaffolding Proteins." International Journal of Molecular Sciences 19, no. 8 (July 29, 2018): 2214. http://dx.doi.org/10.3390/ijms19082214.

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Neuronal activity leads to an influx of Na+ that needs to be rapidly cleared. The sodium-potassium ATPase (Na,K-ATPase) exports three Na+ ions and imports two K+ ions at the expense of one ATP molecule. Na,K-ATPase turnover accounts for the majority of energy used by the brain. To prevent an energy crisis, the energy expense for Na+ clearance must provide an optimal effect. Here we report that in rat primary hippocampal neurons, the clearance of Na+ ions is more efficient if Na,K-ATPase is laterally mobile in the membrane than if it is clustered. Using fluorescence recovery after photobleaching and single particle tracking analysis, we show that the ubiquitous α1 and the neuron-specific α3 catalytic subunits as well as the supportive β1 subunit of Na,K-ATPase are highly mobile in the plasma membrane. We show that cross-linking of the β1 subunit with polyclonal antibodies or exposure to Modulator of Na,K-ATPase (MONaKA), a secreted protein which binds to the extracellular domain of the β subunit, clusters the α3 subunit in the membrane and restricts its mobility. We demonstrate that clustering, caused by cross-linking or by exposure to MONaKA, reduces the efficiency in restoring intracellular Na+. These results demonstrate that extracellular interactions with Na,K-ATPase regulate the Na+ extrusion efficiency with consequences for neuronal energy balance.

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Kinnunen, Patrick C., Gary D. Luker, Kathryn E. Luker, and Jennifer J. Linderman. "Computational modeling implicates protein scaffolding in p38 regulation of Akt." Journal of Theoretical Biology 555 (December 2022): 111294. http://dx.doi.org/10.1016/j.jtbi.2022.111294.

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Fu, Meng-meng, and Erika L. F. Holzbaur. "Integrated regulation of motor-driven organelle transport by scaffolding proteins." Trends in Cell Biology 24, no. 10 (October 2014): 564–74. http://dx.doi.org/10.1016/j.tcb.2014.05.002.

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Robinson, Julia B., Barbara M. Burns, and Deborah Winders Davis. "Maternal scaffolding and attention regulation in children living in poverty." Journal of Applied Developmental Psychology 30, no. 2 (March 2009): 82–91. http://dx.doi.org/10.1016/j.appdev.2008.10.013.

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Lyons, Traci R., Jackie Thorburn, Philip W. Ryan, Andrew Thorburn, Steven M. Anderson, and C. Kenneth Kassenbrock. "Regulation of the Pro-apoptotic Scaffolding Protein POSH by Akt." Journal of Biological Chemistry 282, no. 30 (May 29, 2007): 21987–97. http://dx.doi.org/10.1074/jbc.m704321200.

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Herrero, Ana, David Matallanas, and Walter Kolch. "The spatiotemporal regulation of RAS signalling." Biochemical Society Transactions 44, no. 5 (October 15, 2016): 1517–22. http://dx.doi.org/10.1042/bst20160127.

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Nearly 30% of human tumours harbour mutations in RAS family members. Post-translational modifications and the localisation of RAS within subcellular compartments affect RAS interactions with regulator, effector and scaffolding proteins. New insights into the control of spatiotemporal RAS signalling reveal that activation kinetics and subcellular compartmentalisation are tightly coupled to the generation of specific biological outcomes. Computational modelling can help utilising these insights for the identification of new targets and design of new therapeutic approaches.

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Eckert, Richard L., Mari T. Kaartinen, Maria Nurminskaya, Alexey M. Belkin, Gozde Colak, Gail V. W. Johnson, and Kapil Mehta. "Transglutaminase Regulation of Cell Function." Physiological Reviews 94, no. 2 (April 2014): 383–417. http://dx.doi.org/10.1152/physrev.00019.2013.

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Transglutaminases (TGs) are multifunctional proteins having enzymatic and scaffolding functions that participate in regulation of cell fate in a wide range of cellular systems and are implicated to have roles in development of disease. This review highlights the mechanism of action of these proteins with respect to their structure, impact on cell differentiation and survival, role in cancer development and progression, and function in signal transduction. We also discuss the mechanisms whereby TG level is controlled and how TGs control downstream targets. The studies described herein begin to clarify the physiological roles of TGs in both normal biology and disease states.

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Leith, Georgia, Nicola Yuill, and Alison Pike. "Scaffolding under the microscope: Applying self-regulation and other-regulation perspectives to a scaffolded task." British Journal of Educational Psychology 88, no. 2 (August 29, 2017): 174–91. http://dx.doi.org/10.1111/bjep.12178.

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Riddle, Melissa A., Jennifer M. Hughes, and Benjimen R. Walker. "Role of caveolin-1 in endothelial BKCa channel regulation of vasoreactivity." American Journal of Physiology-Cell Physiology 301, no. 6 (December 2011): C1404—C1414. http://dx.doi.org/10.1152/ajpcell.00013.2011.

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A novel vasodilatory influence of endothelial cell (EC) large-conductance Ca2+-activated K+ (BKCa) channels is present following in vivo exposure to chronic hypoxia (CH) and may exist in other pathological states. However, the mechanism of channel activation that results in altered vasoreactivity is unknown. We tested the hypothesis that CH removes an inhibitory effect of the scaffolding domain of caveolin-1 (Cav-1) on EC BKCa channels to permit activation, thereby affecting vasoreactivity. Experiments were performed on gracilis resistance arteries and ECs from control and CH-exposed (380 mmHg barometric pressure for 48 h) rats. EC membrane potential was hyperpolarized in arteries from CH-exposed rats and arteries treated with the cholesterol-depleting agent methyl-β-cyclodextrin (MBCD) compared with controls. Hyperpolarization was reversed by the BKCa channel antagonist iberiotoxin (IBTX) or by a scaffolding domain peptide of Cav-1 (AP-CAV). Patch-clamp experiments documented an IBTX-sensitive current in ECs from CH-exposed rats and in MBCD-treated cells that was not present in controls. This current was enhanced by the BKCa channel activator NS-1619 and blocked by AP-CAV or cholesterol supplementation. EC BKCa channels displayed similar unitary conductance but greater Ca2+ sensitivity than BKCa channels from vascular smooth muscle. Immunofluorescence imaging demonstrated greater association of BKCa α-subunits with Cav-1 in control arteries than in arteries from CH-exposed rats, although fluorescence intensity for each protein did not differ between groups. Finally, AP-CAV restored myogenic and phenylephrine-induced constriction in arteries from CH-exposed rats without affecting controls. AP-CAV similarly restored diminished reactivity to phenylephrine in control arteries pretreated with MBCD. We conclude that CH unmasks EC BKCa channel activity by removing an inhibitory action of the Cav-1 scaffolding domain that may depend on cellular cholesterol levels.

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Kotelevets, Larissa, and Eric Chastre. "A New Story of the Three Magi: Scaffolding Proteins and lncRNA Suppressors of Cancer." Cancers 13, no. 17 (August 24, 2021): 4264. http://dx.doi.org/10.3390/cancers13174264.

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Scaffolding molecules exert a critical role in orchestrating cellular response through the spatiotemporal assembly of effector proteins as signalosomes. By increasing the efficiency and selectivity of intracellular signaling, these molecules can exert (anti/pro)oncogenic activities. As an archetype of scaffolding proteins with tumor suppressor property, the present review focuses on MAGI1, 2, and 3 (membrane-associated guanylate kinase inverted), a subgroup of the MAGUK protein family, that mediate networks involving receptors, junctional complexes, signaling molecules, and the cytoskeleton. MAGI1, 2, and 3 are comprised of 6 PDZ domains, 2 WW domains, and 1 GUK domain. These 9 protein binding modules allow selective interactions with a wide range of effectors, including the PTEN tumor suppressor, the β-catenin and YAP1 proto-oncogenes, and the regulation of the PI3K/AKT, the Wnt, and the Hippo signaling pathways. The frequent downmodulation of MAGIs in various human malignancies makes these scaffolding molecules and their ligands putative therapeutic targets. Interestingly, MAGI1 and MAGI2 genetic loci generate a series of long non-coding RNAs that act as a tumor promoter or suppressor in a tissue-dependent manner, by selectively sponging some miRNAs or by regulating epigenetic processes. Here, we discuss the different paths followed by the three MAGIs to control carcinogenesis.

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Stephenson, F. A. "Structure and trafficking of NMDA and GABAA receptors." Biochemical Society Transactions 34, no. 5 (October 1, 2006): 877–81. http://dx.doi.org/10.1042/bst0340877.

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The fidelity of synaptic function is dependent on the expression of the appropriate neurotransmitter receptor subtype, the targeting and trafficking of receptors to synapses as well as the regulation of the actual number of receptors at synapses. GABAA (γ-aminobutyric acid type A) receptors and NMDA (N-methyl-D-aspartate) receptors are both examples of ligand-gated, heteromeric neurotransmitter receptors whose cell-surface expression is dynamic and tightly regulated. NMDA receptors are localized at excitatory synapses. These synapses are highly structured but dynamic, with the interplay between NMDA receptors and NMDA receptor-associated scaffolding proteins regulating the expression of functional cell-surface synaptic and extrasynaptic receptors. Based on current information, inhibitory synapses seem to be less ordered, and a GABAA receptor equivalent of PSD-95 (postsynaptic density-95), the scaffolding molecule pivotal to the organization of NMDA receptor complexes at synapses, is yet to be validated. In the present paper, processes regulating the trafficking, assembly and molecular organization of both NMDA receptors and GABAA receptors will be discussed.

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Sauvanet, Cécile, Damien Garbett, and Anthony Bretscher. "The function and dynamics of the apical scaffolding protein E3KARP are regulated by cell-cycle phosphorylation." Molecular Biology of the Cell 26, no. 20 (October 15, 2015): 3615–27. http://dx.doi.org/10.1091/mbc.e15-07-0498.

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We examine the dynamics and function of the apical scaffolding protein E3KARP/NHERF2, which consists of two PDZ domains and a tail containing an ezrin-binding domain. The exchange rate of E3KARP is greatly enhanced during mitosis due to phosphorylation at Ser-303 in its tail region. Whereas E3KARP can substitute for the function of the closely related scaffolding protein EBP50/NHERF1 in the formation of interphase microvilli, E3KARP S303D cannot. Moreover, the S303D mutation enhances the in vivo dynamics of the E3KARP tail alone, whereas in vitro the interaction of E3KARP with active ezrin is unaffected by S303D, implicating another factor regulating dynamics in vivo. A-Raf is found to be required for S303 phosphorylation in mitotic cells. Regulation of the dynamics of EBP50 is known to be dependent on its tail region but modulated by PDZ domain occupancy, which is not the case for E3KARP. Of interest, in both cases, the mechanisms regulating dynamics involve the tails, which are the most diverged region of the paralogues and probably evolved independently after a gene duplication event that occurred early in vertebrate evolution.

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Riddle, Melissa A., and Benjimen R. Walker. "Regulation of endothelial BK channels by heme oxygenase-derived carbon monoxide and caveolin-1." American Journal of Physiology-Cell Physiology 303, no. 1 (July 1, 2012): C92—C101. http://dx.doi.org/10.1152/ajpcell.00356.2011.

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A novel vasodilatory influence of endothelial cell (EC) large-conductance Ca2+-activated K+ (BK) channels is present after in vivo exposure to chronic hypoxia (CH) and may exist in other pathological states. However, the mechanism of channel activation that results in altered vasoreactivity is unknown. Previously, we demonstrated that inhibition of either BK channels or heme oxygenase (HO) restores vasoconstrictor reactivity after CH. Additionally, administration of the scaffolding domain of caveolin (Cav)-1 inhibits EC BK activity and restores vasoconstrictor reactivity in this setting. These results led us to hypothesize that CH exposure results in a loss in Cav-1 inhibition of EC BK channels, resulting in their activation by HO-derived carbon monoxide (CO). Experiments were conducted on freshly dispersed aortic ECs from control and CH-exposed (barometric pressure: 380 mmHg for 48 h) rats. In electrophysiology experiments, outward currents were greater in cells from CH rats as well as from cells from control rats treated with the cholesterol-depleting agent methyl-β-cyclodextrin. These enhanced currents were returned to control by HO inhibition. Channel activity could be restored by the CO donor CO-releasing molecule (CORM)-2 during HO inhibition. Administration of the Cav-1 scaffolding domain eliminated BK currents in cells from CH rats, and current was not restored by the addition of CORM-2. Colocalization experiments in ECs from control and CH rats demonstrated an association between HO-2, Cav-1, and BK. We conclude that EC BK channel activity is HO dependent in the absence of the inhibitory effect of the Cav-1 scaffolding domain.

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Nussinov, Ruth, Buyong Ma, and Chung-Jung Tsai. "A broad view of scaffolding suggests that scaffolding proteins can actively control regulation and signaling of multienzyme complexes through allostery." Biochimica et Biophysica Acta (BBA) - Proteins and Proteomics 1834, no. 5 (May 2013): 820–29. http://dx.doi.org/10.1016/j.bbapap.2012.12.014.

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Lavigne, John V., Karen R. Gouze, Joyce Hopkins, and Fred B. Bryant. "A multidomain cascade model of early childhood risk factors associated with oppositional defiant disorder symptoms in a community sample of 6-year-olds." Development and Psychopathology 28, no. 4pt2 (December 9, 2015): 1547–62. http://dx.doi.org/10.1017/s0954579415001194.

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AbstractThe present study examined a cascade model of age 4 and 5 contextual, parent, parenting, and child factors on symptoms of oppositional defiant disorder (ODD) at age 6 in a diverse community sample of 796 children. Contextual factors include socioeconomic status, family stress, and conflict; parent factors included parental depression; parenting factors included parental hostility, support, and scaffolding skills; child factors included child effortful control (EC), negative affect (NA), and sensory regulation. Direct effects of age 5 conflict, hostility, scaffolding, EC, and NA were found. Significant indirect, cascading effects on age 6 ODD symptom levels were noted for age 4 socioeconomic status via age 5 conflict and scaffolding skills; age 4 parental depression via age 5 child NA; age 4 parental hostility and support via age 5 EC; age 4 support via age 5 EC; and age 4 attachment via age 5 EC. Parenting contributed to EC, and the age 5 EC effects on subsequent ODD symptom levels were distinct from age 5 parental contributions. Scaffolding and ODD symptoms may have a reciprocal relationship. These results highlight the importance of using a multidomain model to examine factors associated with ODD symptoms early in the child's grammar school years.

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Lin, Amy W., and Heng-Ye Man. "Ubiquitination of Neurotransmitter Receptors and Postsynaptic Scaffolding Proteins." Neural Plasticity 2013 (2013): 1–10. http://dx.doi.org/10.1155/2013/432057.

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The human brain is made up of an extensive network of neurons that communicate by forming specialized connections called synapses. The amount, location, and dynamic turnover of synaptic proteins, including neurotransmitter receptors and synaptic scaffolding molecules, are under complex regulation and play a crucial role in synaptic connectivity and plasticity, as well as in higher brain functions. An increasing number of studies have established ubiquitination and proteasome-mediated degradation as universal mechanisms in the control of synaptic protein homeostasis. In this paper, we focus on the role of the ubiquitin-proteasome system (UPS) in the turnover of major neurotransmitter receptors, including glutamatergic and nonglutamatergic receptors, as well as postsynaptic receptor-interacting proteins.

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Tazkia, Savirra, and Tatag Yuli Eko Siswono. "Scaffolding in Supporting Senior High School Students’ Critical Thinking Skills in Sequences and Series Problems." MATHEdunesa 12, no. 1 (June 26, 2023): 207–20. http://dx.doi.org/10.26740/mathedunesa.v12n1.p207-220.

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Critical thinking skills are important for every individual, that they need to be developed in classroom learning, one of which is through learning sequences and series material. However, there are still many students who have difficulty solving problems on sequences and series material, so they need help using scaffolding. This study aims to describe students' thinking skills on sequences and series material, as well as scaffolding which helps students' critical thinking skills in solving sequence and series material questions. The subjects of this study were 2 students who failed to complete the two critical thinking skills tests given. The two students were then interviewed and given scaffolding. The interviews were conducted in a semi-structured manner, that the researcher prepared several questions which could indicate indicators of critical thinking skills, as well as scaffolding which could assist students in solving problems, but the researcher was free to improvise by asking for other information according to the conditions during the interview. The data obtained was then analyzed by reducing the data, presenting the data, and drawing conclusions. The results showed that scaffolding in the form of reviewing played a dominant role for supporting the failure of critical thinking skills on the indicators of interpretation, analysis, evaluation and explanation. Restructuring helps the failure of critical thinking skills on the indicators of interpretation. Explaining helps the failure of critical thinking skills on evaluation indicators. Developing conceptual thinking helps indicators of critical thinking skills analysis, inference, and self-regulation.

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Sun, Jin, and Yixuan Tang. "Maternal scaffolding strategies and early development of self-regulation in Chinese preschoolers." Early Child Development and Care 189, no. 9 (November 2, 2017): 1525–37. http://dx.doi.org/10.1080/03004430.2017.1395874.

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Meyer, Debra K., and Julianne C. Turner. "Using Instructional Discourse Analysis to Study the Scaffolding of Student Self-Regulation." Educational Psychologist 37, no. 1 (March 2002): 17–25. http://dx.doi.org/10.1207/s15326985ep3701_3.

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Lovero, Kathryn L., Yuko Fukata, Adam J. Granger, Masaki Fukata, and Roger A. Nicoll. "The LGI1–ADAM22 protein complex directs synapse maturation through regulation of PSD-95 function." Proceedings of the National Academy of Sciences 112, no. 30 (July 15, 2015): E4129—E4137. http://dx.doi.org/10.1073/pnas.1511910112.

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Synapse development is coordinated by a number of transmembrane and secreted proteins that come together to form synaptic organizing complexes. Whereas a variety of synaptogenic proteins have been characterized, much less is understood about the molecular networks that support the maintenance and functional maturation of nascent synapses. Here, we demonstrate that leucine-rich, glioma-inactivated protein 1 (LGI1), a secreted protein previously shown to modulate synaptic AMPA receptors, is a paracrine signal released from pre- and postsynaptic neurons that acts specifically through a disintegrin and metalloproteinase protein 22 (ADAM22) to set postsynaptic strength. We go on to describe a novel role for ADAM22 in maintaining excitatory synapses through PSD-95/Dlg1/zo-1 (PDZ) domain interactions. Finally, we show that in the absence of LGI1, the mature synapse scaffolding protein PSD-95, but not the immature synapse scaffolding protein SAP102, is unable to modulate synaptic transmission. These results indicate that LGI1 and ADAM22 form an essential synaptic organizing complex that coordinates the maturation of excitatory synapses by regulating the functional incorporation of PSD-95.

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Sathish, Venkatachalem, Binxia Yang, Lucas W. Meuchel, Sarah K. VanOosten, Alexander J. Ryu, Michael A. Thompson, Y. S. Prakash, and Christina M. Pabelick. "Caveolin-1 and force regulation in porcine airway smooth muscle." American Journal of Physiology-Lung Cellular and Molecular Physiology 300, no. 6 (June 2011): L920—L929. http://dx.doi.org/10.1152/ajplung.00322.2010.

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Caveolae are specialized membrane microdomains expressing the scaffolding protein caveolin-1. We recently demonstrated the presence of caveolae in human airway smooth muscle (ASM) and the contribution of caveolin-1 to intracellular calcium ([Ca2+]i) regulation. In the present study, we tested the hypothesis that caveolin-1 regulates ASM contractility. We examined the role of caveolins in force regulation of porcine ASM under control conditions as well as TNF-α-induced airway inflammation. In porcine ASM strips, exposure to 10 mM methyl-β-cyclodextrin (CD) or 5 μM of the caveolin-1 specific scaffolding domain inhibitor peptide (CSD) resulted in time-dependent decrease in force responses to 1 μM ACh. Overnight exposure to the cytokine TNF-α (50 ng/ml) accelerated and increased caveolin-1 expression and enhanced force responses to ACh. Suppression of caveolin-1 with small interfering RNA mimicked the effects of CD or CSD. Regarding mechanisms by which caveolae contribute to contractile changes, inhibition of MAP kinase with 10 μM PD98059 did not alter control or TNF-α-induced increases in force responses to ACh. However, inhibiting RhoA with 100 μM fasudil or 10 μM Y27632 resulted in significant decreases in force responses, with lesser effects in TNF-α exposed samples. Furthermore, Ca2+ sensitivity for force generation was substantially reduced by fasudil or Y27632, an effect even more enhanced in the absence of caveolin-1 signaling. Overall, these results indicate that caveolin-1 is a critical player in enhanced ASM contractility with airway inflammation.

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Diviani, Dario, Kimberly L. Dodge-Kafka, Jinliang Li, and Michael S. Kapiloff. "A-kinase anchoring proteins: scaffolding proteins in the heart." American Journal of Physiology-Heart and Circulatory Physiology 301, no. 5 (November 2011): H1742—H1753. http://dx.doi.org/10.1152/ajpheart.00569.2011.

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The pleiotropic cyclic nucleotide cAMP is the primary second messenger responsible for autonomic regulation of cardiac inotropy, chronotropy, and lusitropy. Under conditions of prolonged catecholaminergic stimulation, cAMP also contributes to the induction of both cardiac myocyte hypertrophy and apoptosis. The formation of localized, multiprotein complexes that contain different combinations of cAMP effectors and regulatory enzymes provides the architectural infrastructure for the specialization of the cAMP signaling network. Scaffolds that bind protein kinase A are called “A-kinase anchoring proteins” (AKAPs). In this review, we discuss recent advances in our understanding of how PKA is compartmentalized within the cardiac myocyte by AKAPs and how AKAP complexes modulate cardiac function in both health and disease.

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Tamanini, Anna, Enrica Fabbri, Tiziana Jakova, Jessica Gasparello, Alex Manicardi, Roberto Corradini, Alessia Finotti, et al. "A Peptide-Nucleic Acid Targeting miR-335-5p Enhances Expression of Cystic Fibrosis Transmembrane Conductance Regulator (CFTR) Gene with the Possible Involvement of the CFTR Scaffolding Protein NHERF1." Biomedicines 9, no. 2 (January 26, 2021): 117. http://dx.doi.org/10.3390/biomedicines9020117.

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(1) Background: Up-regulation of the Cystic Fibrosis Transmembrane Conductance Regulator gene (CFTR) might be of great relevance for the development of therapeutic protocols for cystic fibrosis (CF). MicroRNAs are deeply involved in the regulation of CFTR and scaffolding proteins (such as NHERF1, NHERF2 and Ezrin). (2) Methods: Content of miRNAs and mRNAs was analyzed by RT-qPCR, while the CFTR and NHERF1 production was analyzed by Western blotting. (3) Results: The results here described show that the CFTR scaffolding protein NHERF1 can be up-regulated in bronchial epithelial Calu-3 cells by a peptide-nucleic acid (PNA) targeting miR-335-5p, predicted to bind to the 3′-UTR sequence of the NHERF1 mRNA. Treatment of Calu-3 cells with this PNA (R8-PNA-a335) causes also up-regulation of CFTR. (4) Conclusions: We propose miR-335-5p targeting as a strategy to increase CFTR. While the efficiency of PNA-based targeting of miR-335-5p should be verified as a therapeutic strategy in CF caused by stop-codon mutation of the CFTR gene, this approach might give appreciable results in CF cells carrying other mutations impairing the processing or stability of CFTR protein, supporting its application in personalized therapy for precision medicine.

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Heckhausen, Jutta, and Carsten Wrosch. "Challenges to developmental regulation across the life course." International Journal of Behavioral Development 40, no. 2 (June 4, 2015): 145–50. http://dx.doi.org/10.1177/0165025415588796.

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We discuss the major processes involved in individuals’ motivation and self-regulation of goal striving throughout the life course. While much is regulated based on the biological and societal scaffolding of lifespan development, certain challenges for motivation and self-regulation are more substantial and need to be managed by the individual, providing opportunities for researchers for testing the limits of individual capacities in developmental regulation. These challenging circumstances include major changes in age-graded opportunities for goal pursuit, uncertain or obfuscated opportunities, and major unexpected losses of control. Under such challenging circumstances, the consequences of individual differences in motivational self-regulation, such as optimism, action vs. state orientation, and goal-disengagement capacity are enhanced and may contribute to adaptive patterns of developmental regulation.

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Davis, Michael J., Xin Wu, Timothy R. Nurkiewicz, Junya Kawasaki, Peichun Gui, Michael A. Hill, and Emily Wilson. "Regulation of ion channels by protein tyrosine phosphorylation." American Journal of Physiology-Heart and Circulatory Physiology 281, no. 5 (November 1, 2001): H1835—H1862. http://dx.doi.org/10.1152/ajpheart.2001.281.5.h1835.

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Ion channels are regulated by protein phosphorylation and dephosphorylation of serine, threonine, and tyrosine residues. Evidence for the latter process, tyrosine phosphorylation, has increased substantially since this topic was last reviewed. In this review, we present a comprehensive summary and synthesis of the literature regarding the mechanism and function of ion channel regulation by protein tyrosine kinases and phosphatases. Coverage includes the majority of voltage-gated, ligand-gated, and second messenger-gated channels as well as several types of channels that have not yet been cloned, including store-operated Ca2+ channels, nonselective cation channels, and epithelial Na+ and Cl− channels. Additionally, we discuss the critical roles that channel-associated scaffolding proteins may play in localizing protein tyrosine kinases and phosphatases to the vicinity of ion channels.

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ter Beek, Marlies, Marie-Christine Opdenakker, Alinda W. Spijkerboer, Leonie Brummer, Hidde W. Ozinga, and Jan-Willem Strijbos. "Scaffolding expository history text reading: Effects on adolescents' comprehension, self-regulation, and motivation." Learning and Individual Differences 74 (August 2019): 101749. http://dx.doi.org/10.1016/j.lindif.2019.06.003.

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Grabell, Adam S., Theodore J. Huppert, Frank A. Fishburn, Yanwei Li, Christina O. Hlutkowsky, Hannah M. Jones, Lauren S. Wakschlag, and Susan B. Perlman. "Neural correlates of early deliberate emotion regulation: Young children’s responses to interpersonal scaffolding." Developmental Cognitive Neuroscience 40 (December 2019): 100708. http://dx.doi.org/10.1016/j.dcn.2019.100708.

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Sabourin, J., C. Cognard, and Bruno Constantin. "Regulation by scaffolding proteins of canonical transient receptor potential channels in striated muscle." Journal of Muscle Research and Cell Motility 30, no. 7-8 (December 2009): 289–97. http://dx.doi.org/10.1007/s10974-010-9206-9.

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Mohammadi, Sima, and Hamed Zandi. "Scaffolding Self-Regulation in an Online English Language Course: Utility of Contract Learning." Teaching English as a Second or Foreign Language--TESL-EJ 26, no. 4 (February 1, 2023): 1–33. http://dx.doi.org/10.55593/ej.26104a11.

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As students’ achievement is correlated with self-regulation, finding interventions promoting self-regulated learning (SRL) in online courses is a current focus of research. However, few studies have explored the potential of contract learning in scaffolding and developing SRL in non-traditional learners who have work and family and are at risk of dropout. Here, we investigate the utility of contract learning using a qualitative approach. Using a qualitative approach, we collected data from the experience of one teacher and seven non-traditional learners in an online English for Specific Purposes (ESP) course. The data were collected from teacher logs over eight months and semi-structured interviews with the students. The results of deductive thematic analysis of the data indicate that contract learning positively affected the forethought, performance, and self-reflection phases. Further, despite the cognitive, emotional, external, motivational, and behavioral challenges aggravated by the pandemic, the teacher’s efforts to implement contract learning affected the persistence and effort, goal setting, strategic planning, and time management of most learners (N = 4). Possible reasons for the learners’ success and failure and the implications for developing SRL skills in students at risk of dropout in online English courses are discussed.

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Seo, Yongbo, Seojung Mo, Suhyun Kim, Hyun Kim, and Hae-Chul Park. "Tamalin Function Is Required for the Survival of Neurons and Oligodendrocytes in the CNS." International Journal of Molecular Sciences 23, no. 21 (November 2, 2022): 13395. http://dx.doi.org/10.3390/ijms232113395.

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Tamalin is a post-synaptic scaffolding protein that interacts with group 1 metabotropic glutamate receptors (mGluRs) and several other proteins involved in protein trafficking and cytoskeletal events, including neuronal growth and actin reorganization. It plays an important role in synaptic plasticity in vitro by controlling the ligand-dependent trafficking of group 1 mGluRs. Abnormal regulation of mGluRs in the central nervous system (CNS) is associated with glutamate-mediated neurodegenerative disorders. However, the pathological consequences of tamalin deficiency in the CNS are unclear. In this study, tamalin knockout (KO) zebrafish and mice exhibited neurodegeneration along with oligodendrocyte degeneration in the post-embryonic CNS to adulthood without any developmental defects, thus suggesting the function of tamalin is more important in the postnatal stage to adulthood than that in CNS development. Interestingly, hypomyelination was independent of axonal defects in the CNS of tamalin knockout zebrafish and mice. In addition, the loss of Arf6, a downstream signal of tamalin scaffolding protein, synergistically induced neurodegeneration in tamalin KO zebrafish even in the developing CNS. Furthermore, tamalin KO zebrafish displayed increased mGluR5 expression. Taken together, tamalin played an important role in neuronal and oligodendrocyte survival and myelination through the regulation of mGluR5 in the CNS.

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Castello, Angelo, Michael Engelke, Johannes Tucholski, Thomas Oellerich, Anna Tafuri, Tony Pawson, and Facundo Batista. "Nck proteins are recruited directly to the BCR and regulate PI3K signaling thereby shaping B cell immune responses (P1154)." Journal of Immunology 190, no. 1_Supplement (May 1, 2013): 190.2. http://dx.doi.org/10.4049/jimmunol.190.supp.190.2.

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Abstract Binding of antigen to the B cell antigen receptor (BCR) triggers the activation of different kinases and the initiation of many signaling pathways required for mounting B-dependent immune responses. Scaffolding proteins, recruited downstream of the BCR, act as signal integrators through the recruitment of multiple signaling effectors. Nck is a family of scaffolding proteins best known for linking phosphotyrosine signals to cytoskeleton regulation but until now uncharacterized in the context of B lymphocytes. In our study, Nck was found to be directly recruited to the Igα tail of the BCR and to be important to regulate immune-receptor signaling. Through the generation of a novel Nck1 and Nck2 B cell conditional KO mouse model, we found these adaptors to be essential for mounting T-independent immune response and differentiate into extrafollicular plasma cells during T-dependent responses. The phenotype reported was shown to be due to defective PI3K signaling and Foxo1 downregulation in response to antigen challenge. Our work therefore provides the first compelling evidence for a critical role of Nck in BCR signaling, which is independent of its cytoskeleton regulation yet essential to mount B cell responses.

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Akakura, Shin, and Irwin H. Gelman. "Pivotal Role of AKAP12 in the Regulation of Cellular Adhesion Dynamics: Control of Cytoskeletal Architecture, Cell Migration, and Mitogenic Signaling." Journal of Signal Transduction 2012 (June 28, 2012): 1–7. http://dx.doi.org/10.1155/2012/529179.

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Cellular dynamics are controlled by key signaling molecules such as cAMP-dependent protein kinase (PKA) and protein kinase C (PKC). AKAP12/SSeCKS/Gravin (AKAP12) is a scaffold protein for PKA and PKC which controls actin-cytoskeleton reorganization in a spatiotemporal manner. AKAP12 also acts as a tumor suppressor which regulates cell-cycle progression and inhibits Src-mediated oncogenic signaling and cytoskeletal pathways. Reexpression of AKAP12 causes cell flattening, reorganization of the actin cytoskeleton, and the production of normalized focal adhesion structures. Downregulation of AKAP12 induces the formation of thickened, longitudinal stress fibers and the proliferation of adhesion complexes. AKAP12-null mouse embryonic fibroblasts exhibit hyperactivation of PKC, premature cellular senescence, and defects in cytokinesis, relating to the loss of PKC scaffolding activity by AKAP12. AKAP12-null mice exhibit increased cell senescence and increased susceptibility to carcinogen-induced oncogenesis. The paper describes the regulatory and scaffolding functions of AKAP12 and how it regulates cell adhesion, signaling, and oncogenic suppression.

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Taylor, Sue. "The Modification of Boerkaert’s (1999) Model of Self-Regulation to Include Younger Learners." Frontiers of Contemporary Education 2, no. 1 (April 5, 2021): p22. http://dx.doi.org/10.22158/fce.v2n1p22.

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This study of self-regulation draws on Boerkaert’s (1999) model but proposes adaptations. In particular, it examines the role of the teacher in the promotion of self-regulation, and the importance of curriculum for creating opportunities for autonomous learning. Since Boerkaert’s model was devised for older learners, adaptations are proposed to reflect its possible meaning for younger learners, particularly through the supportive scaffolding of their learning and development toward self-regulation. The study uses an international sample survey of children’s responses to curricular experiences, as well as making comparisons between different educational systems and environments. The article concludes with suggestions for changes in practice to develop self-regulated learners from the early primary years.

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Rodriguez, Anthony B., J. David Peske, Amber N. Woods, and Victor H. Engelhard. "Regulation of peripheral node addressin in tumor-associated CD31+ vascular endothelial cells." Journal of Immunology 196, no. 1_Supplement (May 1, 2016): 212.17. http://dx.doi.org/10.4049/jimmunol.196.supp.212.17.

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Abstract Naïve T cells use peripheral node addressin (PNAd), normally found on lymph node (LN) high endothelial venules (HEV), to traffic into lymphoid organs. We previously reported that the vasculature of murine tumors expressed PNAd and CCL21, which supports infiltration and intratumoral activation of naïve T cells, in turn delaying tumor growth. PNAd expression on tumor vasculature depends on effector CD8+ T cells that secrete LTα3, which signals through TNFR on tumor-associated CD31+ endothelial cells. PNAd expression is low on tumor vasculature, suggesting that it might be regulated differently than PNAd on HEV. Using RT-qPCR, we found that most of the enzymes responsible for PNAd synthesis are expressed comparably in CD31+ cells from tumors and LN. However, the primary sulfotransferase responsible for the generation of the 6-sulfo sialyl Lewis X structure on PNAd HEV, GlcNAc6ST-2, is minimally expressed in tumors. Tumor CD31+ cells expressed equivalent levels of GlcNAc6ST-1, suggesting that it is responsible for low-level PNAd expression. Of the scaffolding proteins that make up PNAd, GlyCAM-1 was minimally expressed in tumor CD31+ cells, whereas all others were expressed comparably. To identify the components of PNAd biosynthesis in tumor CD31+ cells that are controlled by LTα3-TNFR signaling, we evaluated tumors from WT and TNFR1/2KO mice. GlyCAM-1 was the only assessed PNAd component that was ablated in TNFR1/2KO tumors. However, based on transcript levels, GlyCAM-1 accounts for only about 10% of the PNAd scaffolding proteins in tumor CD31+ cells. This suggests that TNFR signaling regulates additional PNAd biosynthetic components yet to be examined, or that it regulates one or more components at the level of protein translation.

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De Rycker, Manu, and Carolyn M. Price. "Tankyrase Polymerization Is Controlled by Its Sterile Alpha Motif and Poly(ADP-Ribose) Polymerase Domains." Molecular and Cellular Biology 24, no. 22 (November 15, 2004): 9802–12. http://dx.doi.org/10.1128/mcb.24.22.9802-9812.2004.

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ABSTRACT Tankyrases are novel poly(ADP-ribose) polymerases that have SAM and ankyrin protein-interaction domains. They are found at telomeres, centrosomes, nuclear pores, and Golgi vesicles and have been shown to participate in telomere length regulation. Their other function(s) are unknown, and it has been difficult to envision a common role at such diverse cellular locations. We have shown that tankyrase 1 polymerizes through its sterile alpha motif (SAM) domain to assemble large protein complexes. In vitro polymerization is reversible and still allows interaction with ankyrin-domain binding proteins. Polymerization can also occur in vivo, with SAM-dependent association of overexpressed tankyrase leading to formation of large tankyrase-containing vesicles, disruption of Golgi structure, and inhibition of apical secretion. Finally, tankyrase polymers are dissociated efficiently by poly(ADP-ribosy)lation. This disassembly is prevented by mutation of the PARP domain. Our findings indicate that tankyrase 1 has the unique capacity to promote both assembly and disassembly of large protein complexes. Thus, tankyrases appear to be master scaffolding proteins that regulate the formation of dynamic protein networks at different cellular locations. This implies a common scaffolding function for tankyrases at each location, with specific tankyrase interaction partners conferring location-specific roles to each network, e.g., telomere compaction or regulation of vesicle trafficking.

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Bushau-Sprinkle, Adrienne M., and Eleanor D. Lederer. "New roles of the Na+/H+ exchange regulatory factor 1 scaffolding protein: a review." American Journal of Physiology-Renal Physiology 318, no. 3 (March 1, 2020): F804—F808. http://dx.doi.org/10.1152/ajprenal.00467.2019.

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Na+/H+ exchange regulatory factor 1 (NHERF1), a member of a PDZ scaffolding protein family, was first identified as an organizer of membrane-bound protein complexes composed of hormone receptors, signal transduction pathways, and electrolyte and mineral transporters and channels. NHERF1 is involved in the regulation of Na+/H+ exchanger 3, Na+-dependent phosphate transporter 2a, and Na+-K+-ATPase through its ability to scaffold these transporters to the plasma membrane, allowing regulation of these protein complexes with their associated hormone receptors. Recently, NHERF1 has received increased interest in its involvement in a variety of functions, including cell structure and trafficking, tumorigenesis and tumor behavior, inflammatory responses, and tissue injury. In this review, we highlight the evidence for the expansive role of NHERF1 in cell biology and speculate on the implications for renal physiology and pathophysiology.

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Verhey, Kristen J., Debra Meyer, Reneé Deehan, John Blenis, Bruce J. Schnapp, Tom A. Rapoport, and Ben Margolis. "Cargo of Kinesin Identified as Jip Scaffolding Proteins and Associated Signaling Molecules." Journal of Cell Biology 152, no. 5 (March 5, 2001): 959–70. http://dx.doi.org/10.1083/jcb.152.5.959.

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The cargo that the molecular motor kinesin moves along microtubules has been elusive. We searched for binding partners of the COOH terminus of kinesin light chain, which contains tetratricopeptide repeat (TPR) motifs. Three proteins were found, the c-jun NH2-terminal kinase (JNK)–interacting proteins (JIPs) JIP-1, JIP-2, and JIP-3, which are scaffolding proteins for the JNK signaling pathway. Concentration of JIPs in nerve terminals requires kinesin, as evident from the analysis of JIP COOH-terminal mutants and dominant negative kinesin constructs. Coprecipitation experiments suggest that kinesin carries the JIP scaffolds preloaded with cytoplasmic (dual leucine zipper–bearing kinase) and transmembrane signaling molecules (the Reelin receptor, ApoER2). These results demonstrate a direct interaction between conventional kinesin and a cargo, indicate that motor proteins are linked to their membranous cargo via scaffolding proteins, and support a role for motor proteins in spatial regulation of signal transduction pathways.

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Journal articles on the topic 'Regulation scaffolding'

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