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Journal articles on the topic 'STUB1'

Author: Grafiati

Published: 10 March 2023

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1

Ullah, Kifayat, Suping Chen, Jiaqi Lu, Xiaohui Wang, Qing Liu, Yang Zhang, Yaqiu Long, Zhanhong Hu, and Guoqiang Xu. "The E3 ubiquitin ligase STUB1 attenuates cell senescence by promoting the ubiquitination and degradation of the core circadian regulator BMAL1." Journal of Biological Chemistry 295, no. 14 (February 10, 2020): 4696–708. http://dx.doi.org/10.1074/jbc.ra119.011280.

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Cell senescence is one of the most important processes determining cell fate and is involved in many pathophysiological conditions, including cancer, neurodegenerative diseases, and other aging-associated diseases. It has recently been discovered that the E3 ubiquitin ligase STIP1 homology and U-box–containing protein 1 (STUB1 or CHIP) is up-regulated during the senescence of human fibroblasts and modulates cell senescence. However, the molecular mechanism underlying STUB1-controlled senescence is not clear. Here, using affinity purification and MS-based analysis, we discovered that STUB1 binds to brain and muscle ARNT-like 1 (BMAL1, also called aryl hydrocarbon receptor nuclear translocator–like protein 1 (ARNTL)). Through biochemical experiments, we confirmed the STUB1-BMAL1 interaction, identified their interaction domains, and revealed that STUB1 overexpression down-regulates BMAL1 protein levels through STUB1's enzymatic activity and that STUB1 knockdown increases BMAL1 levels. Further experiments disclosed that STUB1 enhances BMAL1 degradation, which is abolished upon proteasome inhibition. Moreover, we found that STUB1 promotes the formation of Lys-48–linked polyubiquitin chains on BMAL1, facilitating its proteasomal degradation. Interestingly, we also discovered that oxidative stress promotes STUB1 nuclear translocation and enhances its co-localization with BMAL1. STUB1 expression attenuates hydrogen peroxide–induced cell senescence, indicated by a reduced signal in senescence-associated β-gal staining and decreased protein levels of two cell senescence markers, p53 and p21. BMAL1 knockdown diminishes this effect, and BMAL1 overexpression abolishes STUB1's effect on cell senescence. In summary, the results of our work reveal that the E3 ubiquitin ligase STUB1 ubiquitinates and degrades its substrate BMAL1 and thereby alleviates hydrogen peroxide–induced cell senescence.

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Chen, Dong-Hui, Caitlin Latimer, Mayumi Yagi, Mesaki Kenneth Ndugga-Kabuye, Elyana Heigham, Suman Jayadev, James S. Meabon, et al. "Heterozygous STUB1 missense variants cause ataxia, cognitive decline, and STUB1 mislocalization." Neurology Genetics 6, no. 2 (February 20, 2020): e397. http://dx.doi.org/10.1212/nxg.0000000000000397.

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ObjectiveTo identify the genetic cause of autosomal dominant ataxia complicated by behavioral abnormalities, cognitive decline, and autism in 2 families and to characterize brain neuropathologic signatures of dominant STUB1-related ataxia and investigate the effects of pathogenic variants on STUB1 localization.MethodsClinical and research-based exome sequencing was used to identify the causative variants for autosomal dominant ataxia in 2 families. Gross and microscopic neuropathologic evaluations were performed on the brains of 4 affected individuals in these families.ResultsMutations in STUB1 have been primarily associated with childhood-onset autosomal recessive ataxia, but here we report heterozygous missense variants in STUB1 (p.Ile53Thr and p.The37Leu) confirming the recent reports of autosomal dominant inheritance. Cerebellar atrophy on imaging and cognitive deficits often preceded ataxia. Unique neuropathologic examination of the 4 brains showed the marked loss of Purkinje cells (PCs) without microscopic evidence of significant pathology outside the cerebellum. The normal pattern of polarized somatodendritic STUB1 protein expression in PCs was lost, resulting in aberrant STUB1 localization in the distal PC dendritic arbors.ConclusionsThis study confirms a dominant inheritance pattern in STUB1-ataxia in addition to a recessive one and documents its association with cognitive and behavioral disability, including autism. In the most extensive analysis of cerebellar pathology in this disease, we demonstrate disruption of STUB1 protein in PCs as part of the underlying pathogenesis.

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Pakdaman, Yasaman, Siren Berland, Helene J. Bustad, Sigrid Erdal, Bryony A. Thompson, Paul A. James, Kjersti N. Power, et al. "Genetic Dominant Variants in STUB1, Segregating in Families with SCA48, Display In Vitro Functional Impairments Indistinctive from Recessive Variants Associated with SCAR16." International Journal of Molecular Sciences 22, no. 11 (May 30, 2021): 5870. http://dx.doi.org/10.3390/ijms22115870.

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Variants in STUB1 cause both autosomal recessive (SCAR16) and dominant (SCA48) spinocerebellar ataxia. Reports from 18 STUB1 variants causing SCA48 show that the clinical picture includes later-onset ataxia with a cerebellar cognitive affective syndrome and varying clinical overlap with SCAR16. However, little is known about the molecular properties of dominant STUB1 variants. Here, we describe three SCA48 families with novel, dominantly inherited STUB1 variants (p.Arg51_Ile53delinsProAla, p.Lys143_Trp147del, and p.Gly249Val). All the patients developed symptoms from 30 years of age or later, all had cerebellar atrophy, and 4 had cognitive/psychiatric phenotypes. Investigation of the structural and functional consequences of the recombinant C-terminus of HSC70-interacting protein (CHIP) variants was performed in vitro using ubiquitin ligase activity assay, circular dichroism assay and native polyacrylamide gel electrophoresis. These studies revealed that dominantly and recessively inherited STUB1 variants showed similar biochemical defects, including impaired ubiquitin ligase activity and altered oligomerization properties of the CHIP. Our findings expand the molecular understanding of SCA48 but also mean that assumptions concerning unaffected carriers of recessive STUB1 variants in SCAR16 families must be re-evaluated. More investigations are needed to verify the disease status of SCAR16 heterozygotes and elucidate the molecular relationship between SCA48 and SCAR16 diseases.

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Genis, David, Sara Ortega-Cubero, Hector San Nicolás, Jordi Corral, Josep Gardenyes, Laura de Jorge, Eva López, et al. "Heterozygous STUB1 mutation causes familial ataxia with cognitive affective syndrome (SCA48)." Neurology 91, no. 21 (October 31, 2018): e1988-e1998. http://dx.doi.org/10.1212/wnl.0000000000006550.

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ObjectiveTo describe a new spinocerebellar ataxia (SCA48) characterized by early cerebellar cognitive-affective syndrome (CCAS) and late-onset SCA.MethodsThis is a descriptive study of a family that has been followed for more than a decade with periodic neurologic and neuropsychological examinations, MRI, brain SPECT perfusion, and genetic analysis. Whole exome sequencing was performed in 3 affected and 1 unaffected family member and subsequently validated by linkage analysis of chromosome 16p13.3.ResultsSix patients fully developed cognitive-affective and complete motor cerebellar syndrome associated with vermian and hemispheric cerebellar atrophy, suggesting a continuum from a dysexecutive syndrome slowly evolving to a complete and severe CCAS with late truncal ataxia. Three presymptomatic patients showed focal cerebellar atrophy in the vermian, paravermian, and the medial part of cerebellar lobes VI and VII, suggesting that cerebellar atrophy preceded the ataxia, and that the neurodegeneration begins in cerebellar areas related to cognition and emotion, spreading later to the whole cerebellum. Among the candidate variants, only the frameshift heterozygous c.823_824delCT STUB1 (p.L275Dfs*16) pathogenic variant cosegregated with the disease. The p.L275Dfs*16 heterozygous STUB1 pathogenic variant leads to neurodegeneration and atrophy in cognition- and emotion-related cerebellar areas and reinforces the importance of STUB1 in maintaining cognitive cerebellar function.ConclusionsWe report a heterozygous STUB1 pathogenic genetic variant causing dominant cerebellar ataxia. Since recessive mutations in STUB1 gene have been previously associated with SCAR16, these findings suggest a previously undescribed SCA locus (SCA48; MIM# 618093).

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Lin, Jiacheng, Limin Yin, Xia-Zhen Xu, He-Chen Sun, Zhi-Hua Huang, Xue-Yun Ni, Yan Chen, and Xu Lin. "Bay41-4109-induced aberrant polymers of hepatitis b capsid proteins are removed via STUB1-promoted p62-mediated macroautophagy." PLOS Pathogens 18, no. 1 (January 14, 2022): e1010204. http://dx.doi.org/10.1371/journal.ppat.1010204.

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The hepatitis B virus (HBV) core protein (HBc) functions in multiple steps of the viral life cycle. Heteroaryldihydropyrimidine compounds (HAPs) such as Bay41-4109 are capsid protein allosteric modulators that accelerate HBc degradation and inhibit the virion secretion of HBV, specifically by misleading HBc assembly into aberrant non-capsid polymers. However, the subsequent cellular fates of these HAP-induced aberrant non-capsid polymers are not well understood. Here, we discovered that that the chaperone-binding E3 ubiquitin ligase protein STUB1 is required for the removal of Bay41-4109-induced aberrant non-capsid polymers from HepAD38 cells. Specifically, STUB1 recruits BAG3 to transport Bay41-4109-induced aberrant non-capsid polymers to the perinuclear region of cells, thereby initiating p62-mediated macroautophagy and lysosomal degradation. We also demonstrate that elevating the STUB1 level enhances the inhibitory effect of Bay41-4109 on the production of HBeAg and HBV virions in HepAD38 cells, in HBV-infected HepG2-NTCP cells, and in HBV transgenic mice. STUB1 overexpression also facilitates the inhibition of Bay41-4109 on the cccDNA formation in de novo infection of HBV. Understanding these molecular details paves the way for applying HAPs as a potentially curative regimen (or a component of a combination treatment) for eradicating HBV from hepatocytes of chronic infection patients.

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Turkgenc, Burcu, Burcin Sanlidag, Amber Eker, Aslı Giray, Ozgur Kutuk, Cengiz Yakicier, Aslıhan Tolun, and Sehime G. Temel. "STUB1 polyadenylation signal variant AACAAA does not affect polyadenylation but decreases STUB1 translation causing SCAR16." Human Mutation 39, no. 10 (August 22, 2018): 1344–48. http://dx.doi.org/10.1002/humu.23601.

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Mol, Merel O., Jeroen G. J. van Rooij, Esther Brusse, Annemieke J. M. H. Verkerk, Shamiram Melhem, Wilfred F. A. den Dunnen, Patrizia Rizzu, Chiara Cupidi, John C. van Swieten, and Laura Donker Kaat. "Clinical and pathologic phenotype of a large family with heterozygous STUB1 mutation." Neurology Genetics 6, no. 3 (March 23, 2020): e417. http://dx.doi.org/10.1212/nxg.0000000000000417.

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ObjectiveTo describe the clinical and pathologic features of a novel pedigree with heterozygous STUB1 mutation causing SCA48.MethodsWe report a large pedigree of Dutch decent. Clinical and pathologic data were reviewed, and genetic analyses (whole-exome sequencing, whole-genome sequencing, and linkage analysis) were performed on multiple family members.ResultsPatients presented with adult-onset gait disturbance (ataxia or parkinsonism), combined with prominent cognitive decline and behavioral changes. Whole-exome sequencing identified a novel heterozygous frameshift variant c.731_732delGC (p.C244Yfs*24) in STUB1 segregating with the disease. This variant was present in a linkage peak on chromosome 16p13.3. Neuropathologic examination of 3 cases revealed a consistent pattern of ubiquitin/p62-positive neuronal inclusions in the cerebellum, neocortex, and brainstem. In addition, tau pathology was present in 1 case.ConclusionsThis study confirms previous findings of heterozygous STUB1 mutations as the cause of SCA48 and highlights its prominent cognitive involvement, besides cerebellar ataxia and movement disorders as cardinal features. The presence of intranuclear inclusions is a pathologic hallmark of the disease. Future studies will provide more insight into its pathologic heterogeneity.

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Szpisjak, László, András Salamon, Viola L. Németh, Noémi Szépfalusi, Zoltán Maróti, Tibor Kalmár, Aliz Zimmermann, Dénes Zádori, and Péter Klivényi. "Novel heterozygous STUB1 gene mutation causes SCA48 in a Hungarian patient." Ideggyógyászati szemle 76, no. 1-2 (2023): 63–72. http://dx.doi.org/10.18071/isz.76.0063.

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Spinocerebellar ataxia type 48 (SCA48) is an autosomal dominantly inherited disease characterized by gait and limb ataxia, cerebellar dysarthria, cognitive impairment, psychiatric abnormalities and variable types of movement disorders. To date, more than 30 STUB1 gene (NM_005861.4) mutations have been described in the genetic background of SCA48. The aim of this short report was to demonstrate the first Hungarian SCA48 patient caused by a novel STUB1 missense mutation (c.788G>C, p.Arg263Pro). The characteristics of detailed neurological phenotype, brain MRI and genetic assessment are presented and compared to previously published cases. The most important neurological findings of the patient were gait ataxia, dysarthria, cognitive decline and psychiatric problems including depression, anxiety and mild impulsivity. The brain MRI demonstrated cerebellar atrophy with posterolateral predominance and frontal lobe cortical atrophy. Clinical exome sequencing examination identified the above-mentioned missense variant located in the significant ubiquitinase domain of the CHIP protein. In this paper the first Hungarian SCA48 patient was described with characteristic neuropsychiatric signs and brain MRI abnormalities, due to a novel STUB1 gene missense mutation.

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Cocozza, Sirio, Filippo M. Santorelli, and Giuseppe De Michele. "STUB1 ‐Related Ataxias: A Challenging Diagnosis." Movement Disorders Clinical Practice 7, no. 6 (July 19, 2020): 733–34. http://dx.doi.org/10.1002/mdc3.12992.

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Schuster, S., E. Heuten, A. Velic, J. Admard, M. Synofzik, S. Ossowski, B. Macek, S. Hauser, and L. Schöls. "CHIP mutations affect the heat shock response differently in human fibroblasts and iPSC-derived neurons." Disease Models & Mechanisms 13, no. 10 (October 1, 2020): dmm045096. http://dx.doi.org/10.1242/dmm.045096.

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ABSTRACTC-terminus of HSC70-interacting protein (CHIP) encoded by the gene STUB1 is a co-chaperone and E3 ligase that acts as a key regulator of cellular protein homeostasis. Mutations in STUB1 cause autosomal recessive spinocerebellar ataxia type 16 (SCAR16) with widespread neurodegeneration manifesting as spastic-ataxic gait disorder, dementia and epilepsy. CHIP−/− mice display severe cerebellar atrophy, show high perinatal lethality and impaired heat stress tolerance. To decipher the pathomechanism underlying SCAR16, we investigated the heat shock response (HSR) in primary fibroblasts of three SCAR16 patients. We found impaired HSR induction and recovery compared to healthy controls. HSPA1A/B transcript levels (coding for HSP70) were reduced upon heat shock but HSP70 remained higher upon recovery in patient- compared to control-fibroblasts. As SCAR16 primarily affects the central nervous system we next investigated the HSR in cortical neurons (CNs) derived from induced pluripotent stem cells of SCAR16 patients. We found CNs of patients and controls to be surprisingly resistant to heat stress with high basal levels of HSP70 compared to fibroblasts. Although heat stress resulted in strong transcript level increases of many HSPs, this did not translate into higher HSP70 protein levels upon heat shock, independent of STUB1 mutations. Furthermore, STUB1(−/−) neurons generated by CRISPR/Cas9-mediated genome editing from an isogenic healthy control line showed a similar HSR to patients. Proteomic analysis of CNs showed dysfunctional protein (re)folding and higher basal oxidative stress levels in patients. Our results question the role of impaired HSR in SCAR16 neuropathology and highlight the need for careful selection of proper cell types for modeling human diseases.

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Liu, Chengfei, Cameron M. Armstrong, Shu Ning, Joy C. Yang, Wei Lou, Alan P. Lombard, Jinge Zhao, et al. "ARVib suppresses growth of advanced prostate cancer via inhibition of androgen receptor signaling." Oncogene 40, no. 35 (July 16, 2021): 5379–92. http://dx.doi.org/10.1038/s41388-021-01914-2.

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AbstractTargeting androgen signaling with the second-generation anti-androgen drugs, such as enzalutamide (Enza), abiraterone (Abi), apalutamide (Apal), and darolutamide (Daro), is the mainstay for the treatment of castration-resistant prostate cancer (CRPC). While these treatments are effective initially, resistance occurs frequently. Continued expression of androgen receptor (AR) and its variants such as AR-V7 despite AR-targeted therapy contributes to treatment resistance and cancer progression in advanced CRPC patients. This highlights the need for new strategies blocking continued AR signaling. Here, we identify a novel AR/AR-V7 degrader (ARVib) and found that ARVib effectively degrades AR/AR-V7 protein and attenuates AR/AR-V7 downstream target gene expression in prostate cancer cells. Mechanistically, ARVib degrades AR/AR-V7 protein through the ubiquitin-proteasome pathway mediated by HSP70/STUB1 machinery modulation. ARVib suppresses HSP70 expression and promotes STUB1 nuclear translocation, where STUB1 binds to AR/AR-V7 and promotes its ubiquitination and degradation. ARVib significantly inhibits resistant prostate tumor growth and improves enzalutamide treatment in vitro and in vivo. These data suggest that ARVib has potential for development as an AR/AR-V7 degrader to treat resistant CRPC.

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Shi, Yueli, Xinyu Wang, Zhiyong Xu, Ying He, Chunyi Guo, Lingjuan He, Caijuan Huan, et al. "PDLIM5 inhibits STUB1-mediated degradation of SMAD3 and promotes the migration and invasion of lung cancer cells." Journal of Biological Chemistry 295, no. 40 (July 31, 2020): 13798–811. http://dx.doi.org/10.1074/jbc.ra120.014976.

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Transforming growth factor β (TGFβ) signaling plays an important role in regulating tumor malignancy, including in non–small cell lung cancer (NSCLC). The major biological responses of TGFβ signaling are determined by the effector proteins SMAD2 and SMAD3. However, the regulators of TGFβ–SMAD signaling are not completely revealed yet. Here, we showed that the scaffolding protein PDLIM5 (PDZ and LIM domain protein 5, ENH) critically promotes TGFβ signaling by maintaining SMAD3 stability in NSCLC. First, PDLIM5 was highly expressed in NSCLC compared with that in adjacent normal tissues, and high PDLIM5 expression was associated with poor outcome. Knockdown of PDLIM5 in NSCLC cells decreased migration and invasion in vitro and lung metastasis in vivo. In addition, TGFβ signaling and TGFβ-induced epithelial–mesenchymal transition was repressed by PDLIM5 knockdown. Mechanistically, PDLIM5 knockdown resulted in a reduction of SMAD3 protein levels. Overexpression of SMAD3 reversed the TGFβ-signaling-repressing and anti-migration effects induced by PDLIM5 knockdown. Notably, PDLIM5 interacted with SMAD3 but not SMAD2 and competitively suppressed the interaction between SMAD3 and its E3 ubiquitin ligase STUB1. Therefore, PDLIM5 protected SMAD3 from STUB1-mediated proteasome degradation. STUB1 knockdown restored SMAD3 protein levels, cell migration, and invasion in PDLIM5-knockdown cells. Collectively, our findings indicate that PDLIM5 is a novel regulator of basal SMAD3 stability, with implications for controlling TGFβ signaling and NSCLC progression.

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Olszewska, Diana A., and Justin A. Kinsella. "Reply to STUB1 ‐Related Ataxias: A Challenging Diagnosis." Movement Disorders Clinical Practice 7, no. 6 (July 19, 2020): 735–36. http://dx.doi.org/10.1002/mdc3.12993.

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Choi, Won Hoon, Yejin Yun, Seoyoung Park, Jun Hyoung Jeon, Jeeyoung Lee, Jung Hoon Lee, Su-A. Yang, et al. "Aggresomal sequestration and STUB1-mediated ubiquitylation during mammalian proteaphagy of inhibited proteasomes." Proceedings of the National Academy of Sciences 117, no. 32 (July 28, 2020): 19190–200. http://dx.doi.org/10.1073/pnas.1920327117.

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The 26S proteasome, a self-compartmentalized protease complex, plays a crucial role in protein quality control. Multiple levels of regulatory systems modulate proteasomal activity for substrate hydrolysis. However, the destruction mechanism of mammalian proteasomes is poorly understood. We found that inhibited proteasomes are sequestered into the insoluble aggresome via HDAC6- and dynein-mediated transport. These proteasomes colocalized with the autophagic receptor SQSTM1 and cleared through selective macroautophagy, linking aggresomal segregation to autophagic degradation. This proteaphagic pathway was counterbalanced with the recovery of proteasomal activity and was critical for reducing cellular proteasomal stress. Changes in associated proteins and polyubiquitylation on inhibited 26S proteasomes participated in the targeting mechanism to the aggresome and autophagosome. The STUB1 E3 Ub ligase specifically ubiquitylated purified human proteasomes in vitro, mainly via Lys63-linked chains. Genetic and chemical inhibition of STUB1 activity significantly impaired proteasome processing and reduced resistance to proteasomal stress. These data demonstrate that aggresomal sequestration is the crucial upstream event for proteasome quality control and overall protein homeostasis in mammals.

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Dema, Alessandro, Dörte Faust, Katina Lazarow, Marc Wippich, Martin Neuenschwander, Kerstin Zühlke, Andrea Geelhaar, et al. "Cyclin-Dependent Kinase 18 Controls Trafficking of Aquaporin-2 and Its Abundance through Ubiquitin Ligase STUB1, Which Functions as an AKAP." Cells 9, no. 3 (March 10, 2020): 673. http://dx.doi.org/10.3390/cells9030673.

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Arginine-vasopressin (AVP) facilitates water reabsorption in renal collecting duct principal cells through regulation of the water channel aquaporin-2 (AQP2). The hormone binds to vasopressin V2 receptors (V2R) on the surface of the cells and stimulates cAMP synthesis. The cAMP activates protein kinase A (PKA), which initiates signaling that causes an accumulation of AQP2 in the plasma membrane of the cells facilitating water reabsorption from primary urine and fine-tuning of body water homeostasis. AVP-mediated PKA activation also causes an increase in the AQP2 protein abundance through a mechanism that involves dephosphorylation of AQP2 at serine 261 and a decrease in its poly-ubiquitination. However, the signaling downstream of PKA that controls the localization and abundance of AQP2 is incompletely understood. We carried out an siRNA screen targeting 719 kinase-related genes, representing the majority of the kinases of the human genome and analyzed the effect of the knockdown on AQP2 by high-content imaging and biochemical approaches. The screening identified 13 hits whose knockdown inhibited the AQP2 accumulation in the plasma membrane. Amongst the candidates was the so far hardly characterized cyclin-dependent kinase 18 (CDK18). Our further analysis revealed a hitherto unrecognized signalosome comprising CDK18, an E3 ubiquitin ligase, STUB1 (CHIP), PKA and AQP2 that controls the localization and abundance of AQP2. CDK18 controls AQP2 through phosphorylation at serine 261 and STUB1-mediated ubiquitination. STUB1 functions as an A-kinase anchoring protein (AKAP) tethering PKA to the protein complex and bridging AQP2 and CDK18. The modulation of the protein complex may lead to novel concepts for the treatment of disorders which are caused or are associated with dysregulated AQP2 and for which a satisfactory treatment is not available, e.g., hyponatremia, liver cirrhosis, diabetes insipidus, ADPKD or heart failure.

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Davis, Erica E., Ravikumar Balasubramanian, Zachary A. Kupchinsky, David L. Keefe, Lacey Plummer, Kamal Khan, Blazej Meczekalski, et al. "TCF12 haploinsufficiency causes autosomal dominant Kallmann syndrome and reveals network-level interactions between causal loci." Human Molecular Genetics 29, no. 14 (July 3, 2020): 2435–50. http://dx.doi.org/10.1093/hmg/ddaa120.

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Abstract Dysfunction of the gonadotropin-releasing hormone (GnRH) axis causes a range of reproductive phenotypes resulting from defects in the specification, migration and/or function of GnRH neurons. To identify additional molecular components of this system, we initiated a systematic genetic interrogation of families with isolated GnRH deficiency (IGD). Here, we report 13 families (12 autosomal dominant and one autosomal recessive) with an anosmic form of IGD (Kallmann syndrome) with loss-of-function mutations in TCF12, a locus also known to cause syndromic and non-syndromic craniosynostosis. We show that loss of tcf12 in zebrafish larvae perturbs GnRH neuronal patterning with concomitant attenuation of the orthologous expression of tcf3a/b, encoding a binding partner of TCF12, and stub1, a gene that is both mutated in other syndromic forms of IGD and maps to a TCF12 affinity network. Finally, we report that restored STUB1 mRNA rescues loss of tcf12 in vivo. Our data extend the mutational landscape of IGD, highlight the genetic links between craniofacial patterning and GnRH dysfunction and begin to assemble the functional network that regulates the development of the GnRH axis.

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Ferreira, Joao Vasco, Ana Rosa Soares, José S. Ramalho, Teresa Ribeiro-Rodrigues, Catarina Máximo, Mónica Zuzarte, Henrique Girão, and Paulo Pereira. "Exosomes and STUB1/CHIP cooperate to maintain intracellular proteostasis." PLOS ONE 14, no. 10 (October 15, 2019): e0223790. http://dx.doi.org/10.1371/journal.pone.0223790.

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Tang, Dong‐E, Yong Dai, Lie‐Wen Lin, Yong Xu, Dong‐Zhou Liu, Xiao‐Ping Hong, Hao‐Wu Jiang, and Song‐Hui Xu. "STUB1 suppresseses tumorigenesis and chemoresistance through antagonizing YAP1 signaling." Cancer Science 110, no. 10 (August 28, 2019): 3145–56. http://dx.doi.org/10.1111/cas.14166.

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Shang, Yu, Xinghui Zhao, Bo Tian, Yinyin Wang, Fangli Ren, Baoqing Jia, Yonggong Zhai, Wei Chen, Dacheng He, and Zhijie Chang. "CHIP/Stub1 interacts with eIF5A and mediates its degradation." Cellular Signalling 26, no. 5 (May 2014): 1098–104. http://dx.doi.org/10.1016/j.cellsig.2014.01.030.

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Wang, Shuai, Yi Li, Yun-Hong Hu, Ren Song, Yan Gao, Hai-Yun Liu, Hong-Bing Shu, and Yu Liu. "STUB1 is essential for T-cell activation by ubiquitinating CARMA1." European Journal of Immunology 43, no. 4 (February 15, 2013): 1034–41. http://dx.doi.org/10.1002/eji.201242554.

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Löffek, Stefanie, Stefan Wöll, Jörg Höhfeld, Rudolf E. Leube, Cristina Has, Leena Bruckner-Tuderman, and Thomas M. Magin. "The ubiquitin ligase CHIP/STUB1 targets mutant keratins for degradation." Human Mutation 31, no. 4 (February 11, 2010): 466–76. http://dx.doi.org/10.1002/humu.21222.

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Ravel, Jean-Marie, Mehdi Benkirane, Nadège Calmels, Laëtitia Lambert, Michel Koenig, and Mathilde Renaud. "Extension du spectre clinique de l’ataxie associée aux variations de STUB1." Revue Neurologique 177 (April 2021): S53. http://dx.doi.org/10.1016/j.neurol.2021.02.197.

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Kumar, Dhiraj, and Pravir Kumar. "Integrated Mechanism of Lysine 351, PARK2, and STUB1 in AβPP Ubiquitination." Journal of Alzheimer's Disease 68, no. 3 (April 8, 2019): 1125–50. http://dx.doi.org/10.3233/jad-181219.

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Mamun, Md Mahfuz Al, Muhammad Riaz Khan, Yifu Zhu, Yuwei Zhang, Shuai Zhou, Ran Xu, Ihtisham Bukhari, et al. "Stub1 maintains proteostasis of master transcription factors in embryonic stem cells." Cell Reports 39, no. 10 (June 2022): 110919. http://dx.doi.org/10.1016/j.celrep.2022.110919.

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Depondt, C., S. Donatello, N. Simonis, M. Rai, R. van Heurck, M. Abramowicz, M. D'Hooghe, and M. Pandolfo. "Autosomal recessive cerebellar ataxia of adult onset due to STUB1 Mutations." Neurology 82, no. 19 (April 9, 2014): 1749–50. http://dx.doi.org/10.1212/wnl.0000000000000416.

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Shang, Yu, Xialian Xu, Xiaolin Duan, Junwei Guo, Yinyin Wang, Fangli Ren, Dacheng He, and Zhijie Chang. "Hsp70 and Hsp90 oppositely regulate TGF-β signaling through CHIP/Stub1." Biochemical and Biophysical Research Communications 446, no. 1 (March 2014): 387–92. http://dx.doi.org/10.1016/j.bbrc.2014.02.124.

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Ferreira, João Vasco, Hugo Fôfo, Eloy Bejarano, Carla Figueira Bento, José S. Ramalho, Henrique Girão, and Paulo Pereira. "STUB1/CHIP is required for HIF1A degradation by chaperone-mediated autophagy." Autophagy 9, no. 9 (September 29, 2013): 1349–66. http://dx.doi.org/10.4161/auto.25190.

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Salim, Corinna, Hannah Muders, Andreas Jäger, and Anna Konermann. "Role of chaperone-assisted selective autophagy (CASA) in mechanical stress protection of periodontal ligament cells." Journal of Orofacial Orthopedics / Fortschritte der Kieferorthopädie 83, no. 1 (November 4, 2021): 1–12. http://dx.doi.org/10.1007/s00056-021-00358-3.

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Abstract Objective The periodontal ligament (PDL) is exposed to constant mechanical forces potentiated by orthodontic tooth movement (OTM). The aim of our study was to investigate the involvement of chaperone-assisted selective autophagy (CASA) in mechanosensing and cellular adaption to forces in the PDL. Materials and methods Human PDL cells were loaded with 2.5, 5, and 10% of static mechanical strain for 24 h in vitro. Untreated cells served as controls. Gene expression of HSPA8, HSPB8, BAG3, STUB1, SYNPO2 was investigated via RT-qPCR (Quantitative reverse transcription PCR). Western blot evidenced protein expression of these molecules and of Filamin A. In vivo analyses of CASA were performed via immunohistochemistry on teeth with and without OTM. Results CASA machinery genes were inherently expressed in PDL cells and exhibited transcriptional induction upon mechanical strain. Protein analyses underlined these findings, even though modulation upon force exertion also demonstrated a decrease for some molecules and loading strengths. In vivo results evidenced again the uniform upregulation of HSPA8, HSPB8, BAG3, STUB1, SYNPO2 and Filamin A in teeth with OTM compared to controls. Experiments generally evidenced a pronounced variability in the expression between donors both on the gene and protein level. Conclusions Our study is the first to identify both the expression and functional relevance of CASA in the PDL. The data reflect its probable central role in adequate adaption to forces exerted by OTM and in mechanical stress protection of cells. Deeper knowledge of the CASA pathway will allow better assessment of predisposing factors regarding side effects during mechanical force application that can be used in orthodontic practice.

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Zhang, Yizhi, Zhoujia Chen, Xuerui Luo, Bin Wu, Bin Li, and Bin Wang. "Cimetidine down-regulates stability of Foxp3 protein via Stub1 in Treg cells." Human Vaccines & Immunotherapeutics 12, no. 10 (June 20, 2016): 2512–18. http://dx.doi.org/10.1080/21645515.2016.1191719.

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Gazulla, José, Silvia Izquierdo-Alvarez, Esther Sierra-Martínez, María Eugenia Marta-Moreno, and Sara Alvarez. "Inaugural cognitive decline, late disease onset and novel STUB1 variants in SCAR16." Neurological Sciences 39, no. 12 (September 11, 2018): 2231–33. http://dx.doi.org/10.1007/s10072-018-3545-5.

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Olszewska, Diana A., and Justin A. Kinsella. "Extending the Phenotypic Spectrum Associated with STUB1 Mutations: A Case of Dystonia." Movement Disorders Clinical Practice 7, no. 3 (March 9, 2020): 318–24. http://dx.doi.org/10.1002/mdc3.12914.

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32

Guo, Junwei, Fangli Ren, Yinyin Wang, Shan Li, Zhengrong Gao, Xiaoyan Wang, Hongxiu Ning, et al. "miR-764-5p promotes osteoblast differentiation through inhibition of CHIP/STUB1 expression." Journal of Bone and Mineral Research 27, no. 7 (June 15, 2012): 1607–18. http://dx.doi.org/10.1002/jbmr.1597.

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Del Prete, Dolores, Richard C. Rice, Anjali M. Rajadhyaksha, and Luciano D'Adamio. "Amyloid Precursor Protein (APP) May Act as a Substrate and a Recognition Unit for CRL4CRBN and Stub1 E3 Ligases Facilitating Ubiquitination of Proteins Involved in Presynaptic Functions and Neurodegeneration." Journal of Biological Chemistry 291, no. 33 (June 20, 2016): 17209–27. http://dx.doi.org/10.1074/jbc.m116.733626.

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The amyloid precursor protein (APP), whose mutations cause Alzheimer disease, plays an important in vivo role and facilitates transmitter release. Because the APP cytosolic region (ACR) is essential for these functions, we have characterized its brain interactome. We found that the ACR interacts with proteins that regulate the ubiquitin-proteasome system, predominantly with the E3 ubiquitin-protein ligases Stub1, which binds the NH2 terminus of the ACR, and CRL4CRBN, which is formed by Cul4a/b, Ddb1, and Crbn, and interacts with the COOH terminus of the ACR via Crbn. APP shares essential functions with APP-like protein-2 (APLP2) but not APP-like protein-1 (APLP1). Noteworthy, APLP2, but not APLP1, interacts with Stub1 and CRL4CRBN, pointing to a functional pathway shared only by APP and APLP2. In vitro ubiquitination/ubiquitome analysis indicates that these E3 ligases are enzymatically active and ubiquitinate the ACR residues Lys649/650/651/676/688. Deletion of Crbn reduces ubiquitination of Lys676 suggesting that Lys676 is physiologically ubiquitinated by CRL4CRBN. The ACR facilitated in vitro ubiquitination of presynaptic proteins that regulate exocytosis, suggesting a mechanism by which APP tunes transmitter release. Other dementia-related proteins, namely Tau and apoE, interact with and are ubiquitinated via the ACR in vitro. This, and the evidence that CRBN and CUL4B are linked to intellectual disability, prompts us to hypothesize a pathogenic mechanism, in which APP acts as a modulator of E3 ubiquitin-protein ligase(s), shared by distinct neuronal disorders. The well described accumulation of ubiquitinated protein inclusions in neurodegenerative diseases and the link between the ubiquitin-proteasome system and neurodegeneration make this concept plausible.

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Shi, Lin, Chen Li, Yan Gao, Jing Ye, Yuanan Lu, and Xueqin Liu. "STUB1 activates antiviral response in zebrafish by promoting the expression of RIG-I." Fish & Shellfish Immunology 123 (April 2022): 182–93. http://dx.doi.org/10.1016/j.fsi.2022.02.052.

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35

Cordoba, M., S. Rodriguez-Quiroga, E. M. Gatto, A. Alurralde, and M. A. Kauffman. "Ataxia plus myoclonus in a 23-year-old patient due to STUB1 mutations." Neurology 83, no. 3 (June 13, 2014): 287–88. http://dx.doi.org/10.1212/wnl.0000000000000600.

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36

Guo, Yu, Ming Zhao, and Qianjin Lu. "Transcription factor RFX1 is ubiquitinated by E3 ligase STUB1 in systemic lupus erythematosus." Clinical Immunology 169 (August 2016): 1–7. http://dx.doi.org/10.1016/j.clim.2016.06.003.

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Shashar, Moshe, Mostafa E. Belghasem, Shinobu Matsuura, Joshua Walker, Sean Richards, Faisal Alousi, Keshab Rijal, et al. "Targeting STUB1–tissue factor axis normalizes hyperthrombotic uremic phenotype without increasing bleeding risk." Science Translational Medicine 9, no. 417 (November 22, 2017): eaam8475. http://dx.doi.org/10.1126/scitranslmed.aam8475.

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38

Yonezawa, Taishi, Hirotaka Takahashi, Shiori Shikata, Xiaoxiao Liu, Moe Tamura, Shuhei Asada, Tsuyoshi Fukushima, et al. "The ubiquitin ligase STUB1 regulates stability and activity of RUNX1 and RUNX1–RUNX1T1." Journal of Biological Chemistry 292, no. 30 (May 23, 2017): 12528–41. http://dx.doi.org/10.1074/jbc.m117.785675.

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Rao, Lang, Youbao Sha, and N. Tony Eissa. "The E3 ubiquitin ligase STUB1 regulates autophagy and mitochondrial biogenesis by modulating TFEB activity." Molecular & Cellular Oncology 4, no. 6 (October 23, 2017): e1372867. http://dx.doi.org/10.1080/23723556.2017.1372867.

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Shang, Y., J. He, Y. Wang, Q. Feng, Y. Zhang, J. Guo, J. Li, et al. "CHIP/Stub1 regulates the Warburg effect by promoting degradation of PKM2 in ovarian carcinoma." Oncogene 36, no. 29 (March 27, 2017): 4191–200. http://dx.doi.org/10.1038/onc.2017.31.

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Choi, Soyoun, Soo Ryun Park, Ja-Hyun Jang, and Jong Hyeon Ahn. "Spinocerebellar Ataxia 48 Patient With a Novel De Novo Variant of STUB1." Journal of Clinical Neurology 18, no. 6 (2022): 714. http://dx.doi.org/10.3988/jcn.2022.18.6.714.

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42

Zhang, Z., X. K. Han, and G. M. Ji. "The bandgap controlling by geometrical symmetry design in hybrid phononic crystal." International Journal of Modern Physics B 32, no. 04 (February 2018): 1850034. http://dx.doi.org/10.1142/s0217979218500340.

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The effects of symmetries on the bandgap in a newly designed hybrid phononic crystal plate composed of rubber slab and epoxy resin stub are studied for better controlling of bandgaps. The point group symmetry is changed by changing the orientation of the stub. The translation group symmetry is changed by changing the side length and the height of adjacent stubs. Results show that the point group symmetry and translation group symmetry can be important factors for controlling of the bandgaps of phononic crystal. Wider bandgap is obtained by suitable orientation of the stub. Lower bandgap appears when the differences between the adjacent stubs become bigger in supercell.

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Zhang, Shaoyang, Xuemin Guo, Xiufeng Liu, Zhixiong Zhong, Shulan Yang, and Haihe Wang. "Correction to: Adaptor SH3BGRL promotes breast cancer metastasis through PFN1 degradation by translational STUB1 upregulation." Oncogene 41, no. 8 (December 20, 2021): 1227. http://dx.doi.org/10.1038/s41388-021-02129-1.

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44

Schuster, Stefanie, Srinethe Saravanakumar, Ludger Schöls, and Stefan Hauser. "Generation of a homozygous CRISPR/Cas9-mediated knockout human iPSC line for the STUB1 locus." Stem Cell Research 34 (January 2019): 101378. http://dx.doi.org/10.1016/j.scr.2018.101378.

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45

Liu, Chia-Ming, Cheng-Chia Yu, Taichen Lin, Yi-Wen Liao, Pei-Ling Hsieh, Chuan-Hang Yu, and Shiuan-Shinn Lee. "E3 ligase STUB1 attenuates stemness and tumorigenicity of oral carcinoma cells via transglutaminase 2 regulation." Journal of the Formosan Medical Association 119, no. 10 (October 2020): 1532–38. http://dx.doi.org/10.1016/j.jfma.2020.06.004.

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46

Goločorbin, Stanko. "STATIČKA MKE ANALIZA I ANALIZA OSCILOVANJA STUBA VETROGENERATORA." Zbornik radova Fakulteta tehničkih nauka u Novom Sadu 36, no. 01 (December 25, 2020): 27–30. http://dx.doi.org/10.24867/11am09golocorbin.

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Stubovi vetrogeneratora su jedni od najkompleksnije opterećenih stubova (tornjeva) koji postoje u građevini. Uzimajući u obzir da promenljiva priroda brzine vetra intenzivno menja opterećenje na stub u vidu ekscentričnog momenta. Cilj ovog istraživanja je dobijanje rezultata statičke MKE analize u vidu napona prema kojoj možemo, shodno najvećim naponima, promeniti dizajn samog modela stuba vetrogeneratora. Takođe istraživanjem oscilacija stuba i pronalaženjem sopstvenih kružnih frekvencija oscilovanja dobijamo zanje o brzini obrtaja rotora koju treba da ograničimo da stub ne bi mogao da uđe u rezonantni režim. U radu je prikazana primena metode konačnih elemenata (MKE) pri pronalaženju napona stuba pomoću ABAQUS – softvera i primena teorije oscilacija pri pronalaženju sopstvenih kružnih frekvencija i maksimalnih amplituda pomoću Mathematica – softvera, 3D model korišten za MKE analizu je izrađen u Solidworks – softveru.

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47

Goločorbin, Stanko. "STATIČKA MKE ANALIZA I ANALIZA OSCILOVANJA STUBA VETROGENERATORA." Zbornik radova Fakulteta tehničkih nauka u Novom Sadu 36, no. 01 (December 25, 2020): 27–30. http://dx.doi.org/10.24867/11am09golocorbin.

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Stubovi vetrogeneratora su jedni od najkompleksnije opterećenih stubova (tornjeva) koji postoje u građevini. Uzimajući u obzir da promenljiva priroda brzine vetra intenzivno menja opterećenje na stub u vidu ekscentričnog momenta. Cilj ovog istraživanja je dobijanje rezultata statičke MKE analize u vidu napona prema kojoj možemo, shodno najvećim naponima, promeniti dizajn samog modela stuba vetrogeneratora. Takođe istraživanjem oscilacija stuba i pronalaženjem sopstvenih kružnih frekvencija oscilovanja dobijamo zanje o brzini obrtaja rotora koju treba da ograničimo da stub ne bi mogao da uđe u rezonantni režim. U radu je prikazana primena metode konačnih elemenata (MKE) pri pronalaženju napona stuba pomoću ABAQUS – softvera i primena teorije oscilacija pri pronalaženju sopstvenih kružnih frekvencija i maksimalnih amplituda pomoću Mathematica – softvera, 3D model korišten za MKE analizu je izrađen u Solidworks – softveru.

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48

Sung, Youngje. "Dual-Band Reconfigurable Antenna for Polarization Diversity." International Journal of Antennas and Propagation 2018 (2018): 1–7. http://dx.doi.org/10.1155/2018/6878607.

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This paper proposes a dual-band reconfigurable square-ring antenna with a polarization diversity property. The proposed antenna consists of a square-ring resonator, two stubs with a shorting via, and two PIN diodes. The stub is positioned symmetrically to the left and right of the square-ring resonator, and the square-ring antenna connected to one of two stubs has a dual-band resonance. In this case, both resonant frequencies exhibit linear polarization (LP), and the two polarized waves are perpendicular to each other. The PIN diode selectively connects only one of the two stubs to the square-ring resonator. Thus, the polarization of the proposed antenna changes electrically at the two resonant frequencies. In addition, the frequency ratio (f2/f1) can be easily controlled by changing the length or width of the stub.

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Liu, Xiao, Zhiming Hao, Xin Luo, and Zhengbao Jin. "Experimental Behavior and Modelling of Steel Bolted T-Stub Connections." Buildings 13, no. 3 (February 21, 2023): 575. http://dx.doi.org/10.3390/buildings13030575.

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The paper comprehensively investigates the tension performance of Q355 steel T-stubs, whose nonlinear mechanical behavior is modelled by spring-slider elements. First, tension tests were conducted on seven specimens to explore the tension performance of Q355 steel T-stubs. T-stub connections were discussed in terms of their tension characteristics. Second, a numerical simulation was performed to analyze the stress distribution of T-stub components during deformation. Finally, on the basis of the tension characteristics of the T-stub connections, we constructed the constitutive model’s density function. The constitutive model’s force–displacement relationship was derived mathematically. A method for determining parameters was also developed. With the proposed model, the entire tensile behavior of T-stub connections can be described accurately while reducing the degrees of freedom at the contact interfaces, resulting in more efficient computing. Four parameters are defined physically in the model, and their values can be determined directly by macroscopic experiments.

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Li, Ke, Tao Dong, and Zhenghuan Xia. "Wideband Printed Wide-Slot Antenna with Fork-Shaped Stub." Electronics 8, no. 3 (March 21, 2019): 347. http://dx.doi.org/10.3390/electronics8030347.

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This paper presents a multiple-resonance technique that sought to achieve a wide bandwidth for printed wide-slot antennas with fork-shaped stubs. By properly appending an extra fork-shaped stub onto the main fork-shaped stub, the impedance bandwidth was able to be clearly broadened. To validate this technique, two designs where the extra stubs were added at different positions of the main stub were constructed. The measured impedance bandwidths of the proposed antennas reached 148.6% (0.9–6.1 GHz) for S11 < −10 dB, indicating a 17.9% wider bandwidth than that of the normal antenna (0.9–4.3 GHz). Moreover, a stable radiation pattern was observed within the operating frequency range. The proposed antennas were confirmed to be much-improved candidates for applications in various wireless communication systems.

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