Relevant bibliographies by topics / FMR1 protein

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Academic literature on the topic 'FMR1 protein'

Author: Grafiati
Published: 3 June 2025
Last updated: 31 July 2025

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Journal articles on the topic "FMR1 protein"

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Khandjian, Edouard W. "Biology of the fragile X mental retardation protein, an RNA-binding protein." Biochemistry and Cell Biology 77, no. 4 (1999): 331–42. http://dx.doi.org/10.1139/o99-035.

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The fragile X syndrome, an X-linked disease, is the most frequent cause of inherited mental retardation. The syndrome results from the absence of expression of the FMR1 gene (fragile mental retardation 1) owing to the expansion of a CGG trinucleotide repeat located in the 5prime untranslated region of the gene and the subsequent methylation of its CpG island. The FMR1 gene product (FMRP) is a cytoplasmic protein that contains two KH domains and one RGG box, characteristics of RNA-binding proteins. FMRP is associated with mRNP complexes containing poly(A)+mRNA within actively translating polyri
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Nguyen, Xuan Phuoc, Adriana Vilkaite, Ulrike Bender, et al. "Regulation of Bone Morphogenetic Protein Receptor Type II Expression by FMR1/Fragile X Mental Retardation Protein in Human Granulosa Cells in the Context of Poor Ovarian Response." International Journal of Molecular Sciences 25, no. 19 (2024): 10643. http://dx.doi.org/10.3390/ijms251910643.

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Fragile X mental retardation protein (FMRP) is a translational repressor encoded by FMR1. It targets bone morphogenetic protein receptor type II (BMPR2), which regulates granulosa cell (GC) function and follicle development. However, whether this interaction affects folliculogenesis remains unclear. Therefore, this study investigated the potential effect of FMRP-BMPR2 dysregulation in ovarian reserves and infertility. COV434 cells and patient-derived GCs were used to evaluate FMRP and BMPR2 expression. Similarly, FMR1, BMPR2, LIMK1, and SMAD expression were evaluated in GCs with normal (NOR) a
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Nosyreva, Elena D., and Kimberly M. Huber. "Metabotropic Receptor-Dependent Long-Term Depression Persists in the Absence of Protein Synthesis in the Mouse Model of Fragile X Syndrome." Journal of Neurophysiology 95, no. 5 (2006): 3291–95. http://dx.doi.org/10.1152/jn.01316.2005.

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Fragile X syndrome (FXS), a form of human mental retardation, is caused by loss of function mutations in the fragile X mental retardation gene ( FMR1). The protein product of FMR1, fragile X mental retardation protein (FMRP) is an RNA-binding protein and may function as a translational suppressor. Metabotropic glutamate receptor–dependent long-term depression (mGluR-LTD) in hippocampal area CA1 is a form of synaptic plasticity that relies on dendritic protein synthesis. mGluR-LTD is enhanced in the mouse model of FXS, Fmr1 knockout (KO) mice, suggesting that FMRP negatively regulates translati
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Zhang, Jing, Lingfei Hou, Eric Klann, and David L. Nelson. "Altered Hippocampal Synaptic Plasticity in the Fmr1 Gene Family Knockout Mouse Models." Journal of Neurophysiology 101, no. 5 (2009): 2572–80. http://dx.doi.org/10.1152/jn.90558.2008.

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Fragile X syndrome (FXS) is the most common form of inherited mental retardation. The syndrome results from the absence of the fragile X mental retardation protein (FMRP), which is encoded by the fragile X mental retardation 1 ( FMR1) gene. FMR1 and its two paralogs, fragile X–related genes 1 and 2 ( FXR1 and -2), form the Fmr1 gene family. Here, we examined long-lasting synaptic plasticity in Fmr1 knockout, Fxr2 knockout, and Fmr1/ Fxr2 double knockout mice. We found that metabotropic glutamate receptor–dependent long-term depression (mGluR-LTD) in the hippocampus was affected in Fmr1 knockou
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Saré, Rachel, Christopher Figueroa, Abigail Lemons, Inna Loutaev, and Carolyn Beebe Smith. "Comparative Behavioral Phenotypes of Fmr1 KO, Fxr2 Het, and Fmr1 KO/Fxr2 Het Mice." Brain Sciences 9, no. 1 (2019): 13. http://dx.doi.org/10.3390/brainsci9010013.

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Fragile X syndrome (FXS) is caused by silencing of the FMR1 gene leading to loss of the protein product fragile X mental retardation protein (FMRP). FXS is the most common monogenic cause of intellectual disability. There are two known mammalian paralogs of FMRP, FXR1P, and FXR2P. The functions of FXR1P and FXR2P and their possible roles in producing or modulating the phenotype observed in FXS are yet to be identified. Previous studies have revealed that mice lacking Fxr2 display similar behavioral abnormalities as Fmr1 knockout (KO) mice. In this study, we expand upon the behavioral phenotype
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Randol, Jamie L., Kyoungmi Kim, Matthew D. Ponzini, et al. "Variation of FMRP Expression in Peripheral Blood Mononuclear Cells from Individuals with Fragile X Syndrome." Genes 15, no. 3 (2024): 356. http://dx.doi.org/10.3390/genes15030356.

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Fragile X syndrome (FXS) is the most common heritable cause of intellectual disability and autism spectrum disorder. The syndrome is often caused by greatly reduced or absent protein expression from the fragile X messenger ribonucleoprotein 1 (FMR1) gene due to expansion of a 5′-non-coding trinucleotide (CGG) element beyond 200 repeats (full mutation). To better understand the complex relationships among FMR1 allelotype, methylation status, mRNA expression, and FMR1 protein (FMRP) levels, FMRP was quantified in peripheral blood mononuclear cells for a large cohort of FXS (n = 154) and control
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Siomi, M. C., Y. Zhang, H. Siomi, and G. Dreyfuss. "Specific sequences in the fragile X syndrome protein FMR1 and the FXR proteins mediate their binding to 60S ribosomal subunits and the interactions among them." Molecular and Cellular Biology 16, no. 7 (1996): 3825–32. http://dx.doi.org/10.1128/mcb.16.7.3825.

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Fragile X syndrome, the most common form of hereditary mental retardation, usually results from lack of expression of the FMR1 gene. The FMR1 protein is a cytoplasmic RNA-binding protein. The RNA-binding activity of FMR1 is an essential feature of FMR1, as fragile X syndrome can also result from the expression of mutant FMR1 protein that is impaired in RNA binding. Recently, we described two novel cytoplasmic proteins, FXR1 and FXR2, which are both very similar in amino acid sequence to FMR1 and which also interact strongly with FMR1 and with each other. To understand the function of FMR1 and
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Budimirovic, Dejan B., Annette Schlageter, Stela Filipovic-Sadic, et al. "A Genotype-Phenotype Study of High-Resolution FMR1 Nucleic Acid and Protein Analyses in Fragile X Patients with Neurobehavioral Assessments." Brain Sciences 10, no. 10 (2020): 694. http://dx.doi.org/10.3390/brainsci10100694.

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Fragile X syndrome (FXS) is caused by silencing of the FMR1 gene, which encodes a protein with a critical role in synaptic plasticity. The molecular abnormality underlying FMR1 silencing, CGG repeat expansion, is well characterized; however, delineation of the pathway from DNA to RNA to protein using biosamples from well characterized patients with FXS is limited. Since FXS is a common and prototypical genetic disorder associated with intellectual disability (ID) and autism spectrum disorder (ASD), a comprehensive assessment of the FMR1 DNA-RNA-protein pathway and its correlations with the neu
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Bale, Shyam Sundhar, Nima Saeidi, Srivatsan Kidambi, Martin L. Yarmush, and Monica Casali. "FMR1 Deficiency Alters Self-Renewal and Proliferation of Mouse Embryonic Cells." Nano LIFE 05, no. 02 (2015): 1550003. http://dx.doi.org/10.1142/s1793984415500038.

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The regulation of embryonic stem (ES) cell self-renewal and pluripotency is based upon highly orchestrated transcription factor networks. RNA inhibition has been demonstrated to affect ES cell function by altering gene expression levels that are critical to the maintenance and differentiation of ES cells. Fragile X mental retardation protein (FMRP) is a selective RNA-binding protein that can act as a translational repressor for bound mRNA and regulates the expression of a variety of gene transcripts in numerous adult cells. The absence of FMRP results in the most common form of inherited intel
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Kumari, Daman, Inbal Gazy, and Karen Usdin. "Pharmacological Reactivation of the Silenced FMR1 Gene as a Targeted Therapeutic Approach for Fragile X Syndrome." Brain Sciences 9, no. 2 (2019): 39. http://dx.doi.org/10.3390/brainsci9020039.

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More than ~200 CGG repeats in the 5′ untranslated region of the FMR1 gene results in transcriptional silencing and the absence of the FMR1 encoded protein, FMRP. FMRP is an RNA-binding protein that regulates the transport and translation of a variety of brain mRNAs in an activity-dependent manner. The loss of FMRP causes dysregulation of many neuronal pathways and results in an intellectual disability disorder, fragile X syndrome (FXS). Currently, there is no effective treatment for FXS. In this review, we discuss reactivation of the FMR1 gene as a potential approach for FXS treatment with an
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Dissertations / Theses on the topic "FMR1 protein"

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Hall, Deborah A. "Prevalence of FMR1 repeat expansions in movement disorders /." Connect to abstract via ProQuest. Full text is not available online, 2008. http://proquest.umi.com/pqdweb?did=1545571851&sid=1&Fmt=6&clientId=18952&RQT=309&VName=PQD.

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Thesis (Ph.D. in Clinical Science) -- University of Colorado Denver, 2008.<br>Typescript. Includes bibliographical references (leaves 59-67). Free to UCD Anschutz Medical Campus. Online version available via ProQuest Digital Dissertations;
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Verheij, Coleta. "Characterization of the FMR1 protein involved in the fragile X syndrome." [S.l.] : Rotterdam : [The Author] ; Erasmus University [Host], 1996. http://hdl.handle.net/1765/13734.

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Banerjee, Paromita. "Modeling the Effects of FMR1 Alleles on Behavioral and Synaptic Plasticity." Miami University / OhioLINK, 2008. http://rave.ohiolink.edu/etdc/view?acc_num=miami1217359939.

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Velloso, Fernando Janczur. "Variabilidade do domínio KH-2 da proteína do retardo mental do X frágil (FMRP)." Universidade de São Paulo, 2013. http://www.teses.usp.br/teses/disponiveis/41/41131/tde-21032014-090729/.

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A proteína do retardo mental do X frágil (FMRP), codificada pelo gene do Retardo Mental do X Frágil (do inglês, Fragile Mental Retardation 1, FMR1) tem expressão significativa no encéfalo, gônadas e células proliferativas. A FMRP é uma proteína ligante de RNA, repressora traducional, que transita entre o núcleo celular, grânulos citoplasmáticos e polissomos. Sua associação a RNA pode se dar pelos domínios Tudor N-terminais, dois domínios centrais, com homologia à heteronucleoproteína K (KH) ou motivos RGG, ricos em arginina (R) e glicina (G), C-terminais. A abolição da expressão da FMRP por mu
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ZALFA, FRANCESCA. "A new mechanism for regulating mRNA translation in the mammalian CNS:." Doctoral thesis, Università degli Studi di Roma "Tor Vergata", 2006. http://hdl.handle.net/2108/245.

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Abstract tesi PhD Dr. Zalfa Francesca A new mechanism for regulating mRNA translation in the mammalian CNS: a role for the Fragile X Mental Retardation Protein FMRP (Fragile X Mental Retardation Protein) è una proteina che lega gli RNA altamente espressa nel cervello. L’assenza o la mutazione di FMRP causa la sindrome dell’X fragile, una disfunzione dominante legata al cromosoma X e la più frequente causa di ritardo mentale ereditario (con un’incidenza di 1 su 4000 maschi e di 1 su 6000 femmine). Utilizzando il modello murino della sindrome dell’X Fragile (il topo FMR1 knock-out), h
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Khayachi, Anouar. "Rôles fonctionnels de la SUMOylation de FMRP « Fragile X Mental Retardation Protein »." Thesis, Nice, 2015. http://www.theses.fr/2015NICE4031.

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Le syndrome de l’X-fragile est la forme la plus fréquente de déficience intellectuelle héréditaire liée au chromosome X. Cette maladie résulte de la mutation du gène FMR1 localisé sur le chromosome X. La protéine correspondante, FMRP, est absente chez les patients atteints de la maladie. Il faut noter ici qu’il existe un modèle murin mimant la pathologie humaine. Ainsi dans ces animaux qui n’expriment pas la protéine FMRP, les neurones présentent des anomalies architecturales de la synapse entraînant d’importants dysfonctionnements dans la transmission et la plasticité synaptique qui sont à l’
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NAPOLI, ILARIA. "How the fragile X mental retardation protein represses protein synthesis: a mechanism of translational control in dendrites." Doctoral thesis, Università degli Studi di Roma "Tor Vergata", 2009. http://hdl.handle.net/2108/765.

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La Sindrome dell'X Fragile è la forma di ritardo mentale ereditario più frequente nella popolazione con un'incidenza 1/4000 nei maschi e 1/6000 nelle femmine. La patologia è causata da mutazioni nel gene FMR1 il cui prodotto proteico, FMRP, è altamente espresso nei neuroni. FMRP è una proteina che lega gli RNA messaggeri neuronali e si localizza lungo i dendriti e gli assoni dei neuroni dove controlla il trasporto e la sintesi proteica dei messaggeri associati. Nel presente progetto abbiamo analizzato il meccanismo attraverso il quale FMRP regola la sintesi proteica alle sinapsi, caratteri
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Khayachi, Anouar. "Rôles fonctionnels de la SUMOylation de FMRP « Fragile X Mental Retardation Protein »." Electronic Thesis or Diss., Nice, 2015. http://www.theses.fr/2015NICE4031.

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Le syndrome de l’X-fragile est la forme la plus fréquente de déficience intellectuelle héréditaire liée au chromosome X. Cette maladie résulte de la mutation du gène FMR1 localisé sur le chromosome X. La protéine correspondante, FMRP, est absente chez les patients atteints de la maladie. Il faut noter ici qu’il existe un modèle murin mimant la pathologie humaine. Ainsi dans ces animaux qui n’expriment pas la protéine FMRP, les neurones présentent des anomalies architecturales de la synapse entraînant d’importants dysfonctionnements dans la transmission et la plasticité synaptique qui sont à l’
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Wu, Yuhong. "Structural studies of Human Caprin Protein." OpenSIUC, 2019. https://opensiuc.lib.siu.edu/dissertations/1652.

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Human Caprin-1 and Caprin-2 are prototypic members of the caprin (cytoplasmic activation/proliferation-associated protein) protein family. Vertebrate caprin proteins contain two highly conserved homologous regions (HR1 and HR2) and C-terminal RGG motifs. Drosophila caprin (dCaprin) shares HR1 and RGG motifs but lacks HR2. Caprin-1 and Caprin-2 have important and non-redundant functions. The detailed molecular mechanisms of their actions remain largely unknown.
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Stöcker, Stefanie [Verfasser]. "Function of the Cytoplasmic FMRP Interacting Protein 1 (CyFIP1) in mouse / Stefanie Stöcker." Bonn : Universitäts- und Landesbibliothek Bonn, 2016. http://d-nb.info/1132711193/34.

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Books on the topic "FMR1 protein"

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Walsh, Richard A. Parkinson’s Disease or Essential Tremor? Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190607555.003.0016.

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Fragile X-associated tremor ataxia syndrome is a heredodegenerative syndrome that presents in older men as a tremor syndrome with less prominent ataxia and cognitive impairment initially. The underlying genetic cause, a premutation in the FMR1 gene, results in a toxic accumulation of mRNA. The full mutation, a triple-repeat expansion of more than 200 CGG repeats, gives rise to a reduction in FMR1 protein expression and fragile X, a neurodevelopmental disorder that may be identified in successive male generations. The prevalence of carrier status is high in the general population, and it is lik
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Bagni, Claudia, and Eric Klann. Molecular Functions of the Mammalian Fragile X Mental Retardation Protein: Insights Into Mental Retardation and Synaptic Plasticity. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199744312.003.0008.

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Chapter 8 discusses how Fragile X syndrome (FXS) is caused by the absence of the RNA-binding protein fragile X mental retardation protein (FMRP). FMRP is highly expressed in the brain and gonads, the two organs mainly affected in patients with the syndrome. Functionally, FMRP belongs to the family of RNA-binding proteins, shuttling from the nucleus to the cytoplasm, and, as shown for other RNA-binding proteins, forms large messenger ribonucleoparticles.
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Book chapters on the topic "FMR1 protein"

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Price, Theodore J., and Ohannes K. Melemedjian. "Fragile X Mental Retardation Protein (FMRP) and the Spinal Sensory System." In Results and Problems in Cell Differentiation. Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-21649-7_4.

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Das, Amit, Simanti Bhattacharya, Angshuman Bagchi, and Rakhi Dasgupta. "Understanding the Interaction of Human Formin Binding Protein 4 with Formin FMN1." In Advances in Intelligent Systems and Computing. Springer India, 2015. http://dx.doi.org/10.1007/978-81-322-2247-7_12.

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Garber, Kathryn B., Daniel Gruskin,, and Stephen T. Warren. "FMR1 and the Fragile X Syndrome." In Inborn Errors Of Development. Oxford University PressNew York, NY, 2008. http://dx.doi.org/10.1093/oso/9780195306910.003.0126.

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Abstract Fragile X syndrome (FXS) is an X-linked dominant disorder with reduced penetrance whose primary manifestation is moderate-to- severe mental retardation. It is most often caused by the transcriptional silencing of the FMR1 gene due to an expansion of a CGG-repeat found in the 5’ untranslated region (UTR). This allelic class, with greater than 200 CGG-repeats, is referred to as the full mutation. Normal alleles have up to 54 repeats with the 30 repeats being most common. Intermediate between normal and full mutation alleles are the premutation alleles with 55–200 repeats. Premutation al
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Mastergeorge, Ann M., and Jacky Au. "Fragile X: A Family of Disorders." In Cognitive and Behavioral Abnormalities of Pediatric Diseases. Oxford University Press, 2010. http://dx.doi.org/10.1093/oso/9780195342680.003.0024.

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Fragile X syndrome (FXS) is the most common cause of inherited intellectual disability known, and it is the most common single gene disorder associated with autism (Belmonte and Bourgeron 2006; Reddy 2005). It is caused by the lack or deficiency of the FMR1 protein, FMRP (Loesch et al. 2004b). The typical physical features of FXS include prominent ears, hyperextensible finger joints, flat feet, soft skin, and in adolescence and adulthood large testicles (macroorchidism) and a long face (Hagerman 2002b). The behavioral features include poor eye contact, hyperarousal to stimuli, anxiety, hyperac
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"Fragile X Syndrome: Public Education." In Fragile X Syndrome. Exon Publications, 2024. http://dx.doi.org/10.36255/fragile-x-syndrome-public-education.

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Fragile X Syndrome is a genetic condition that affects both males and females, leading to developmental delays, intellectual disabilities, and behavioral challenges. This article offers a comprehensive overview of the disorder, explaining its genetic causes, symptoms, diagnosis, and management in clear and simple terms. Fragile X Syndrome results from mutations in the FMR1 gene, which disrupts the production of a protein critical for normal brain development. With information tailored to patients, families, and caregivers, this book covers the impact of Fragile X Syndrome on daily life and pro
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Suhl, Joshua, and Charles Hoeffer. "RNA and Protein Targets of FMRP." In Fragile X Syndrome. Elsevier, 2017. http://dx.doi.org/10.1016/b978-0-12-804461-2.00008-1.

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"Contributors." In BSAVA/SAMSoc Guide to Responsible Use of Antibacterials: PROTECT ME. British Small Animal Veterinary Association, 2018. http://dx.doi.org/10.22233/9781910443644.fm1.

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"Contributors." In BSAVA/SAMSoc Guide to Responsible Use of Antibiotics: PROTECT ME (2024). British Small Animal Veterinary Association, 2024. http://dx.doi.org/10.22233/9781913859312.fm1.

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Bansal, Videsha, Amruthavarshini M. S., and K. Jayasankara Reddy. "The Role of Technology in Advancing Psychoneuroimmunology Research." In Advances in Medical Diagnosis, Treatment, and Care. IGI Global, 2024. https://doi.org/10.4018/979-8-3693-7432-0.ch018.

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This chapter explores the transformative impact of technology on Psychoneuroimmunology (PNI), emphasizing advancements in neuroimaging, genomics, and proteomics. Techniques like functional MRI (fMRI) and Positron Emission Tomography (PET) have revolutionized our understanding of brain activity and neuroinflammation. Next-generation sequencing (NGS) and proteomic profiling have unveiled genetic and protein biomarkers linked to stress and immune responses. Wearable technology and mobile health apps now enable continuous monitoring and personalized stress management. Big data analytics and machin
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Levitan, Irwin B., and Leonard K. Kaczmarek. "Formation, Maintenance, and Plasticity of Chemical Synapses." In The Neuron. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199773893.003.0017.

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When developing axons reach their appropriate postsynaptic target, they stop elongating. A series of characteristic morphological and biochemical changes, culminating in synapse formation, then occur. Among the cues used by an excitatory neuron in choosing its correct postsynaptic partner are chemical labels such as Ephrins and Eph receptors. Not all synapses that form during development persist in adult animals. Certain synapses are selectively stabilized; others are lost. In many cases such rearrangements follow a Hebbian rule, whereby excitatory synapses are stabilized when they trigger pos
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Conference papers on the topic "FMR1 protein"

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Jerald, Baby, Gopalakriahnan Nair T R, and Ekambaram Rajasekaran. "Evaluation of the Structural disorder of the protein FMR1 with Carbon Composition." In Annual International Conference on Advances in Biotechnology. Global Science and Technology Forum (GSTF), 2012. http://dx.doi.org/10.5176/2251-2489_bicb06.

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Gonçalves, Aline, Paulo Bazan, Maria da Graça Martins, et al. "FUNCTIONAL CONNECTIVITY IN MILD GNITIVE IMPAIRMENT PATIENTS WITH PIB+ AND – BIOMARKERS." In XIII Meeting of Researchers on Alzheimer's Disease and Related Disorders. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1980-5764.rpda040.

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Background: According to the recent NIA-AA, a probable predictor of Alzheimer’s disease convertor in mild cognitive impairment (MCI) is the Aβ protein deposit in PET PIB exam. However, there is a lack of studies investigating functional connectivity in PIB +/- MCI patients. Objectives: to investigate differences in functional connectivity during resting state in MCI patients with PET PIB+ and - biomarkers. Methods: PET PIB+ (N=12 and PIB- (N=12) MCI patients underwent fMRI during resting state using 3 ROIS related to memory (posterior cingulate and bilateral hippocampus). Results: there were s
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Ludewig, H., M. Todosow, N. Simos, S. Shapiro, and J. Hastings. "Very High Flux Steady State Reactor and Accelerator Based Sources." In 12th International Conference on Nuclear Engineering. ASMEDC, 2004. http://dx.doi.org/10.1115/icone12-49442.

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With the number of steady state neutron sources in the US declining (including the demise of the BNL HFBR) the remaining intense sources are now in Europe (i.e. reactors - ILL and FMR, accelerator - PSI). The intensity of the undisturbed thermal flux for sources currently in operation ranges from1014 n/cm2-s to 1015 n/cm2-s. The proposed Advanced Neutron Source (ANS) was to be a high power reactor (∼ 350 MW) with a projected undisturbed thermal flux of 7×1015 n/cm2-s but never materialized. The objective of the current study is to explore the requirements and implications of two source concept
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