Relevant bibliographies by topics / WDR41

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  2. Dissertations / Theses
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  4. Conference papers

Academic literature on the topic 'WDR41'

Author: Grafiati
Published: 7 July 2024
Last updated: 31 July 2025

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Journal articles on the topic "WDR41"

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Amick, Joseph, Arun Kumar Tharkeshwar, Catherine Amaya,, and Shawn M. Ferguson. "WDR41 supports lysosomal response to changes in amino acid availability." Molecular Biology of the Cell 29, no. 18 (2018): 2213–27. http://dx.doi.org/10.1091/mbc.e17-12-0703.

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C9orf72 mutations are a major cause of amyotrophic lateral sclerosis and frontotemporal dementia. The C9orf72 protein undergoes regulated recruitment to lysosomes and has been broadly implicated in control of lysosome homeostasis. However, although evidence strongly supports an important function for C9orf72 at lysosomes, little is known about the lysosome recruitment mechanism. In this study, we identify an essential role for WDR41, a prominent C9orf72 interacting protein, in C9orf72 lysosome recruitment. Analysis of human WDR41 knockout cells revealed that WDR41 is required for localization
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Talaia, Gabriel, Joseph Amick, and Shawn M. Ferguson. "Receptor-like role for PQLC2 amino acid transporter in the lysosomal sensing of cationic amino acids." Proceedings of the National Academy of Sciences 118, no. 8 (2021): e2014941118. http://dx.doi.org/10.1073/pnas.2014941118.

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PQLC2, a lysosomal cationic amino acid transporter, also serves as a sensor that responds to scarcity of its substrates by recruiting a protein complex composed of C9orf72, SMCR8, and WDR41 to the surface of lysosomes. This protein complex controls multiple aspects of lysosome function. Although it is known that this response to changes in cationic amino acid availability depends on an interaction between PQLC2 and WDR41, the underlying mechanism for the regulated interaction is not known. In this study, we present evidence that the WDR41–PQLC2 interaction is mediated by a short peptide motif
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Tang, Dan, Jingwen Sheng, Liangting Xu, et al. "Cryo-EM structure of C9ORF72–SMCR8–WDR41 reveals the role as a GAP for Rab8a and Rab11a." Proceedings of the National Academy of Sciences 117, no. 18 (2020): 9876–83. http://dx.doi.org/10.1073/pnas.2002110117.

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A massive intronic hexanucleotide repeat (GGGGCC) expansion in C9ORF72 is a genetic origin of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). Recently, C9ORF72, together with SMCR8 and WDR41, has been shown to regulate autophagy and function as Rab GEF. However, the precise function of C9ORF72 remains unclear. Here, we report the cryogenic electron microscopy (cryo-EM) structure of the human C9ORF72–SMCR8–WDR41 complex at a resolution of 3.2 Å. The structure reveals the dimeric assembly of a heterotrimer of C9ORF72–SMCR8–WDR41. Notably, the C-terminal tail of C9ORF72 and
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SHARMA, NISHA, REVANASIDDU D, SUSHIL KUMAR, et al. "Influence of WDR41 and ANKRD31 gene polymorphism on udder and teat type traits and mastitis in Karan Fries cows." Indian Journal of Animal Sciences 92, no. 2 (2022): 215–21. http://dx.doi.org/10.56093/ijans.v92i2.122096.

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In the present study, the effect of genetic polymorphism of WD-repeat containing protein 41 (WDR41) and Ankyrin repeat domain containing protein 31 (ANKRD31) gene on 17 traits related to udder and teat type and mastitis in 123 Karan Fries cows was studied. Restriction Fragment Length Polymorphism (RFLP) was used to identify the SNP (410 bp and 475 bp) in PCR amplified product of intron 4 and exon 10 in WDR41 gene. Both of them were polymorphic with Guanine to Adenine transition, and three genotypes namely AA, AG and GG were observed. In ANKRD31 gene, RFLP was used to identify the SNP in 513 bp
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McAlpine, William, Lei Sun, Kuan-wen Wang, et al. "Excessive endosomal TLR signaling causes inflammatory disease in mice with defective SMCR8-WDR41-C9ORF72 complex function." Proceedings of the National Academy of Sciences 115, no. 49 (2018): E11523—E11531. http://dx.doi.org/10.1073/pnas.1814753115.

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The SMCR8-WDR41-C9ORF72 complex is a regulator of autophagy and lysosomal function. Autoimmunity and inflammatory disease have been ascribed to loss-of-function mutations of Smcr8 or C9orf72 in mice. In humans, autoimmunity has been reported to precede amyotrophic lateral sclerosis caused by mutations of C9ORF72. However, the cellular and molecular mechanisms underlying autoimmunity and inflammation caused by C9ORF72 or SMCR8 deficiencies remain unknown. Here, we show that splenomegaly, lymphadenopathy, and activated circulating T cells observed in Smcr8−/− mice were rescued by triple knockout
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Tang, Dan, Jingwen Sheng, Liangting Xu, Chuangye Yan, and Shiqian Qi. "The C9orf72-SMCR8-WDR41 complex is a GAP for small GTPases." Autophagy 16, no. 8 (2020): 1542–43. http://dx.doi.org/10.1080/15548627.2020.1779473.

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Fukatsu, Shoya, Hinami Sashi, Remina Shirai, et al. "Rab11a Controls Cell Shape via C9orf72 Protein: Possible Relationships to Frontotemporal Dementia/Amyotrophic Lateral Sclerosis (FTDALS) Type 1." Pathophysiology 31, no. 1 (2024): 100–116. http://dx.doi.org/10.3390/pathophysiology31010008.

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Abnormal nucleotide insertions of C9orf72, which forms a complex with Smith–Magenis syndrome chromosomal region candidate gene 8 (SMCR8) protein and WD repeat-containing protein 41 (WDR41) protein, are associated with an autosomal-dominant neurodegenerative frontotemporal dementia and/or amyotrophic lateral sclerosis type 1 (FTDALS1). The differentially expressed in normal and neoplastic cells (DENN) domain-containing C9orf72 and its complex with SMCR8 and WDR41 function as a guanine-nucleotide exchange factor for Rab GTP/GDP-binding proteins (Rab GEF, also called Rab activator). Among Rab pro
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Liu, Kai, Youli Jian, Xiaojuan Sun, et al. "Negative regulation of phosphatidylinositol 3-phosphate levels in early-to-late endosome conversion." Journal of Cell Biology 212, no. 2 (2016): 181–98. http://dx.doi.org/10.1083/jcb.201506081.

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Phosphatidylinositol 3-phosphate (PtdIns3P) plays a central role in endosome fusion, recycling, sorting, and early-to-late endosome conversion, but the mechanisms that determine how the correct endosomal PtdIns3P level is achieved remain largely elusive. Here we identify two new factors, SORF-1 and SORF-2, as essential PtdIns3P regulators in Caenorhabditis elegans. Loss of sorf-1 or sorf-2 leads to greatly elevated endosomal PtdIns3P, which drives excessive fusion of early endosomes. sorf-1 and sorf-2 function coordinately with Rab switching genes to inhibit synthesis of PtdIns3P, allowing its
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Snyder, Anthony J., Andrew T. Abad, and Pranav Danthi. "A CRISPR-Cas9 screen reveals a role for WD repeat-containing protein 81 (WDR81) in the entry of late penetrating viruses." PLOS Pathogens 18, no. 3 (2022): e1010398. http://dx.doi.org/10.1371/journal.ppat.1010398.

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Successful initiation of infection by many different viruses requires their uptake into the endosomal compartment. While some viruses exit this compartment early, others must reach the degradative, acidic environment of the late endosome. Mammalian orthoreovirus (reovirus) is one such late penetrating virus. To identify host factors that are important for reovirus infection, we performed a CRISPR-Cas9 knockout (KO) screen that targets over 20,000 genes in fibroblasts derived from the embryos of C57/BL6 mice. We identified seven genes (WDR81, WDR91, RAB7, CCZ1, CTSL, GNPTAB, and SLC35A1) that w
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LIU, Nan, and ChongLin YANG. "WDR91-WDR81 complex-dependent endolysosomal trafficking and neural development." SCIENTIA SINICA Vitae 49, no. 7 (2019): 798–805. http://dx.doi.org/10.1360/ssv-2019-0100.

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Dissertations / Theses on the topic "WDR41"

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Pietri, David. "Structure and function of the C9ORF72-SMCR8-WDR41 complex and its implication for Amyotrophic Lateral Sclerosis (ALS)." Electronic Thesis or Diss., Strasbourg, 2023. http://www.theses.fr/2023STRAJ087.

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La sclérose latérale amyotrophique (SLA ou maladie de Charcot) est la troisième maladie neurodégénérative la plus répandue. La principale cause génétique de la SLA est une expansion de répétitions GGGGCC dans le gène C9ORF72, dont la protéine forme un complexe avec les protéines SMCR8 et WDR41. Afin de mieux comprendre ses fonctions moléculaires, résoudre sa structure était un objectif principal de ma thèse. En parallèle, nous avons découvert que C9ORF72 régule un mécanisme nouvellement décrit de biogenèse de nouveaux lysosomes nommé reformation autophagique des lysosomes (ALR). Ce processus a
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Kannan, Meghna. "Etude du rôle de WDR47 dans le système nerveux central." Thesis, Strasbourg, 2016. http://www.theses.fr/2016STRAJ086/document.

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Nos travaux sur 26 gènes de la famille des WDR a permis d’en identifier sept (Atg16l1, Coro1c, Dmxl2, Herc1, Kif21b, Wdr47, Wdr89) associés à des anomalies cérébrales majeures. Cette grande famille de protéines reste pourtant peu explorée quant à ses rôles dans le développement du système nerveux central. Nous avons choisi d’étudier WDR47, dont la fonction est totalement inconnue en dépit d’une très grande similarité structurale avec LIS1, protéine à l’origine de la lissencéphalie. En combinant trois modèles expérimentaux (souris, siRNA et levure), nous avons démontré que Wdr47 est essentiel p
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Carpentieri, Jacopo Amerigo. "La mutation WDR81 causant la microcéphalie modifie le trafic endosomique d'EGFR et conduit à une prolifération des cellules progénitrices réduite." Electronic Thesis or Diss., Université Paris sciences et lettres, 2020. https://theses.hal.science/tel-03510180.

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La microlissencéphalie est une malformation cérébrale congénitale caractérisée par la juxtaposition d’un phénotype de microcéphalie (petit cerveau) et de lissencéphalie (cerveau lisse). Nos collaborateurs ont récemment identifié des mutations responsables de cette pathologie dans le gène WDR81 humain. WDR81 est une protéine peu caractérisée et impliquée dans la maturation des endosomes, via la régulation de Pi3K. L'objectif de mon projet de thèse est de caractériser la fonction de WDR81 dans le cerveau en développement et d'identifier comment la mutation de ce gène peut conduire à un développe
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McGillewie, L. "Identification of novel ligands of WDR47, using yeast two-hybrid analysis." Thesis, Stellenbosch : University of Stellenbosch, 2009. http://hdl.handle.net/10019.1/3002.

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Thesis (MScMedSc (Biomedical Sciences. Molecular Biology and Human Genetics. Medical Biochemistry))--University of Stellenbosch, 2009.<br>The mammalian neocortex contributes to the increasing functional complexity of the mammalian brain, partly because of its striking organisation into distinct neuronal layers. The development of the neocortex has been well studied because disrupted neurodevelopment results in several human diseases. The basic principles of neocortical development have been well established for some time; however the molecular mechanisms have only recently been identified.
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Roos, Marna. "Elucidating the role of WDR47 in regulating neuronal migration, autophagy and tubulin dynamics." Thesis, Stellenbosch : Stellenbosch University, 2014. http://hdl.handle.net/10019.1/96065.

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Thesis (MSc)--Stellenbosch University, 2014.<br>ENGLISH ABSTRACT: Introduction Normal cerebral cortex development depends on extensive neuronal migration during embryogenesis, permitting the formation of accurate synaptic circuits and a highly ordered laminar neocortex. The motility of a migrating neuron is achieved by a dynamic microtubule cytoskeleton that alternates between states of stabilization/lengthening and destabilization/shortening. This dynamic instability of the microtubule cytoskeleton is controlled by numerous microtubule-stabilizing and -destabilising proteins that bind di
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平井, 悠哉. "スキャフォールドタンパク質WDR46の核小体サブドメイン形成における役割". 京都大学 (Kyoto University), 2013. http://hdl.handle.net/2433/180535.

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Gonçalves, Jussara Maria. "Análise da expressão imuno-histoquímica das proteínas P53, USP1 e WDR48 com os dados clínico-histopatológicos em carcinomas epidermóides intrabucais." reponame:Repositório Institucional da UFSC, 2016. https://repositorio.ufsc.br/xmlui/handle/123456789/167929.

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Dissertação (mestrado) - Universidade Federal de Santa Catarina, Centro de Ciências da Saúde, Programa de Pós-Graduação em Odontologia, Florianópolis, 2016.<br>Made available in DSpace on 2016-09-20T04:36:04Z (GMT). No. of bitstreams: 1 339917.pdf: 1826007 bytes, checksum: 243c62e86307b651b7169fb44f9ec134 (MD5) Previous issue date: 2016<br>Para inibir a diferenciação e manter as características das células-tronco, proteínas inibidoras da ligação de DNA (ID) antagonizam os fatores de transcrição basic helix-loop-helix (bHLH). A ubiquitinização da proteína ID ocorre em diferentes tecidos, mas
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Tschentscher, Anne [Verfasser], Sabine [Gutachter] Hoffjan, and Moritz [Gutachter] Meins. "Analyse der \(\it WDR45\) und \(\it C19orf12\) Gene bei Neurodegeneration mit Eisenansammlung im Gehirn / Anne Tschentscher ; Gutachter: Sabine Hoffjan, Moritz Meins." Bochum : Ruhr-Universität Bochum, 2017. http://d-nb.info/1133361781/34.

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Abidi, Affef. "Contribution à l'étude des encéphalopathies épileptiques précoces : recherche de nouvelles causes génétiques & caractérisation fonctionnelle des mutations du gène KCNQ2." Thesis, Aix-Marseille, 2016. http://www.theses.fr/2016AIXM5009/document.

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Les Encéphalopathies Épileptiques Précoces sont des pathologies rares et sévères caractérisées par des crises fréquentes commençant dans les trois premiers mois de vie accompagnées d’un EEG intercritique altéré et un pronostic très défavorable. Au cours de la caractérisation génétique d’une cohorte de 402 patients, nous avons mis en évidence une délétion de 19,9 kb localisée en Xp11.23 chez un garçon et 34 mutations de novo du gène KCNQ2. La première partie de mon projet a consisté en l’étude de la pathogénicité de la délétion Xp11.23, qui implique trois gènes dont WDR45. Les mutations de WRD4
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Cavallin, Mara. "Physiopathologie moléculaire et cellulaire des anomalies du développement du cortex cérébral : le syndrome d'Aicardi WDR81 mutations cause extreme microcephaly and impair mitotic progression in human fibroblasts and Drosophila neural stem cells TLE1, a key player in neurogenesis, a new candidate gene for autosomal recessive postnatal microcephaly Mutations in TBR1 gene leads to cortical malformations and intellectual disability Aicardi syndrome: Exome, genome and RNA-sequencing of a large cohort of 19 patients failed to detect the genetic cause Recurrent RTTN mutation leading to severe microcephaly, polymicrogyria and growth restriction Recurrent KIF2A mutations are responsible for classic lissencephaly Recurrent KIF5C mutation leading to frontal pachygyria without microcephaly Rare ACTG1 variants in fetal microlissencephaly De novo TUBB2B mutation causes fetal akinesia deformation sequence with microlissencephaly: An unusual presentation of tubulinopathy A novel recurrent LIS1 splice site mutation in classic lissencephaly Further refinement of COL4A1 and COL4A2 related cortical malformations Prenatal and postnatal presentations of corpus callosum agenesis with polymicrogyria caused By EGP5 mutation Delineating FOXG1 syndrome from congenital microcephaly to hyperkinetic encephalopathy Delineating FOXG1 syndrome: From congenital microcephaly to hyperkinetic encephalopathy." Thesis, Sorbonne Paris Cité, 2019. https://wo.app.u-paris.fr/cgi-bin/WebObjects/TheseWeb.woa/wa/show?t=2213&f=18201.

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Les malformations du cortex cérébral (MDC) représentent une cause importante de handicap et d'épilepsie pharmaco-résistante. Le séquençage à haut débit a permis une amélioration considérable de l'identification des bases moléculaires des MDC non syndromiques. Toutefois, certaines formes, notamment les MDC complexes, demeurent inexpliquées. Mon projet de thèse a pour objectif de progresser dans la compréhension des MDC complexes en utilisant deux modèles : les microlissencéphalies (MLIS) et le syndrome d'Aicardi (AIC), une forme syndromique particulière associant des malformations de l'oeil et
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Book chapters on the topic "WDR41"

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Izawa, S., S. Taniguchi, K. Matsuzawa, et al. "Anti-WDR1 Antibody: A Novel Biochemical Marker for the Differential Diagnosis of Thyroid Neoplasm." In The Endocrine Society's 92nd Annual Meeting, June 19–22, 2010 - San Diego. Endocrine Society, 2010. http://dx.doi.org/10.1210/endo-meetings.2010.part1.p11.p1-550.

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Conference papers on the topic "WDR41"

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Weinert, C. M., C. Schmidt, and H. G. Weber. "Application of asynchronous amplitude histograms for performance monitoring of RZ signals." In Optical Fiber Communication Conference. OSA, 2001. http://dx.doi.org/10.1364/ofc.2001.wdd41.

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Ortigosa-Blanch, A., J. C. Knight, and P. St J. Russell. "Pulse dynamics in polarisation-maintaining photonic crystal fibers." In International Conference on Ultrafast Phenomena. OSA, 2002. http://dx.doi.org/10.1364/up.2002.wd41.

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Iizuka, Takeshi, and Yuri S. Kivshar. "Optical Gap Solitons in Nonresonant Quadratic Media." In Nonlinear Guided Waves and Their Applications. OSA, 1999. http://dx.doi.org/10.1364/nlgw.1999.wd41.

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Seki, Takahiro, Takashi Tamaki, Ryo-ichi Fukuda, Makoto Yokoi, and Hideo Hiramatsu. "Photoinduced Alignment Behaviors of a Nematic Liquid Crystal on Azobenzene Langmuir-Blodgett Monolayers." In Spectral Hole-Burning and Related Spectroscopies: Science and Applications. Optica Publishing Group, 1994. http://dx.doi.org/10.1364/shbs.1994.wd41.

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Trans/cis photoisomerization of azobenzene (Az) molecular films on the substrate is capable of inducing homeotropic/planar alignment changes of nematic liquid crystals (LCs). These photofunctional surfaces are called "command surfaces." (Fig.1)1 The Langmuir-Blodgett (LB) technique provides importance information on the design of the surface layer. The LB film preparation condition should influence, to a large extent, the aligning behavior of the nematic LC as formerly proposed by Hiltrop and Stegemeyer.2 The present work is undertaken to elucidate the relationship between the conditions of th
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Greulich, N., A. Abicht, and N. Heußinger. "WDR45-Associated BPAN: A Rare Cause for Infantile-Onset Seizures and Expressive Language Disorder in a 26-Month-Old Girl." In Abstracts of the 46th Annual Meeting of the Society for Neuropediatrics. Georg Thieme Verlag KG, 2021. http://dx.doi.org/10.1055/s-0041-1739626.

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