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Relevant bibliographies by topics / Clustered protocadherins

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Academic literature on the topic 'Clustered protocadherins'

Author: Grafiati

Published: 5 June 2025

Last updated: 24 June 2025

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Journal articles on the topic "Clustered protocadherins"

1

Chen, W. V., and T. Maniatis. "Clustered protocadherins." Development 140, no. 16 (2013): 3297–302. http://dx.doi.org/10.1242/dev.090621.

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Ravi, Vydianathan, Wei-Ping Yu, Nisha E. Pillai, et al. "Cyclostomes Lack Clustered Protocadherins." Molecular Biology and Evolution 33, no. 2 (2015): 311–15. http://dx.doi.org/10.1093/molbev/msv252.

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Walujkar, Sanket P., Raul Araya-Sechhi, and Marcos Sotomayor. "Simulated Forced Unbinding of Clustered Protocadherins." Biophysical Journal 112, no. 3 (2017): 449a. http://dx.doi.org/10.1016/j.bpj.2016.11.2406.

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4

Nicoludis, John M., Anna G. Green, Sanket Walujkar, et al. "Interaction specificity of clustered protocadherins inferred from sequence covariation and structural analysis." Proceedings of the National Academy of Sciences 116, no. 36 (2019): 17825–30. http://dx.doi.org/10.1073/pnas.1821063116.

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Clustered protocadherins, a large family of paralogous proteins that play important roles in neuronal development, provide an important case study of interaction specificity in a large eukaryotic protein family. A mammalian genome has more than 50 clustered protocadherin isoforms, which have remarkable homophilic specificity for interactions between cellular surfaces. A large antiparallel dimer interface formed by the first 4 extracellular cadherin (EC) domains controls this interaction. To understand how specificity is achieved between the numerous paralogs, we used a combination of structural and computational approaches. Molecular dynamics simulations revealed that individual EC interactions are weak and undergo binding and unbinding events, but together they form a stable complex through polyvalency. Strongly evolutionarily coupled residue pairs interacted more frequently in our simulations, suggesting that sequence coevolution can inform the frequency of interaction and biochemical nature of a residue interaction. With these simulations and sequence coevolution, we generated a statistical model of interaction energy for the clustered protocadherin family that measures the contributions of all amino acid pairs at the interface. Our interaction energy model assesses specificity for all possible pairs of isoforms, recapitulating known pairings and predicting the effects of experimental changes in isoform specificity that are consistent with literature results. Our results show that sequence coevolution can be used to understand specificity determinants in a protein family and prioritize interface amino acid substitutions to reprogram specific protein–protein interactions.

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Jin, Yongfeng, and Hao Li. "Revisiting Dscam diversity: lessons from clustered protocadherins." Cellular and Molecular Life Sciences 76, no. 4 (2018): 667–80. http://dx.doi.org/10.1007/s00018-018-2951-4.

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Han, Meng-Hsuan, Chengyi Lin, Shuxia Meng, and Xiaozhong Wang. "Proteomics Analysis Reveals Overlapping Functions of Clustered Protocadherins." Molecular & Cellular Proteomics 9, no. 1 (2009): 71–83. http://dx.doi.org/10.1074/mcp.m900343-mcp200.

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7

Lefebvre, Julie L. "Neuronal territory formation by the atypical cadherins and clustered protocadherins." Seminars in Cell & Developmental Biology 69 (September 2017): 111–21. http://dx.doi.org/10.1016/j.semcdb.2017.07.040.

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8

Flaherty, Erin, and Tom Maniatis. "The role of clustered protocadherins in neurodevelopment and neuropsychiatric diseases." Current Opinion in Genetics & Development 65 (December 2020): 144–50. http://dx.doi.org/10.1016/j.gde.2020.05.041.

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Goodman, Kerry Marie, Rotem Rubinstein, Chan Aye Thu та ін. "Structural Basis of Diverse Homophilic Recognition by Clustered α- and β-Protocadherins". Neuron 90, № 4 (2016): 709–23. http://dx.doi.org/10.1016/j.neuron.2016.04.004.

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Biswas, S., M. R. Emond та J. D. Jontes. "The clustered protocadherins Pcdhα and Pcdhγ form a heteromeric complex in zebrafish". Neuroscience 219 (вересень 2012): 280–89. http://dx.doi.org/10.1016/j.neuroscience.2012.05.058.

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Dissertations / Theses on the topic "Clustered protocadherins"

1

Modak, Debadrita. "Structural and biochemical studies of non-clustered protocadherins." The Ohio State University, 2020. http://rave.ohiolink.edu/etdc/view?acc_num=osu1595567250446369.

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Gray, Michelle Elizabeth. "Towards Understanding the Cell Adhesion Mediated by Non-clustered Non-classical Protocadherins." The Ohio State University, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=osu1605887233542288.

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Gray, Michelle Elizabeth. "Towards Understanding the Cell Adhesion Mediated by Non-clustered Non-classical Protocadherins." The Ohio State University, 2021. http://rave.ohiolink.edu/etdc/view?acc_num=osu1605887233542288.

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4

Hu, Jiang. "Investigating the role of Smchd1 in control of clustered protocadherin expression." Thesis, Queensland University of Technology, 2016. https://eprints.qut.edu.au/96573/1/Jiang_Hu_Thesis.pdf.

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Smchd1 (Structural Maintenance of Chromosomes Hinge Domain containing 1), a previously uncharacterised gene, was identified during an N-ethyl-nitrosourea (ENU) mutagenesis screen in mice, which was designed to identify modifiers of epigenetic reprogramming. The mutant allele of Smchd1 is named MommeD1 (Modifier of murine metastable epialleles, D1) and results in significantly reduced Smchd1 transcript levels, due to nonsense mediated mRNA decay. Accumulating studies have revealed that Smchd1 plays a critical role in X inactivation, as well as regulating a subset of clustered autosomal genes which are subject to monoallelic expression (e.g. imprinted genes and the clustered protocadherin genes). Loss of SMCHD1 function is also implicated in Facioscapulohumeral Muscular Dystrophy Type 2 (FSHD2) in humans. The clustered protocadherin (Pcdh) genes are expressed in a random combinatorial monoallelic manner and encode cell surface adhesion proteins. The enormous diversity of the protocadherins extracellular domain, which is displayed on the surface of neurons is sufficient to confer each with an individual identity. It has been proposed that this individual identity is critical for forming the cellular connections and interactions necessary to develop complex neuronal networks. Several studies have suggested that the clustered Pcdh genes may play a critical role in autism and schizophrenia. In this project, neural stem cells (NSCs) were used to perform qRT-PCR in bulk cells and at the single cell level to analyse expression of the clustered Pcdh genes, as well as conducting Transcriptome-seq and MBD-seq (methyl-CpG binding domain (MBD)). Results showed that the expression of most clustered Pcdha and Pcdhb isoforms were up-regulated in Smchd1MommeD1/MommeD1 NSCs, and at the individual cell level, more Smchd1MommeD1/MommeD1 NSCs expressed more individual Pcdha and b isoforms per cell than was found in Smchd1+/+ NSCs. Attempts were made to isolate single Purkinje cells from the cerebella of Smchd1+/+ and Smchd1MommeD1/MommeD1 male mice, and analyse the expression of clustered Pcdh genes by single cell qRT-PCR. Unfortunately, the methods used to isolate single Purkinje cells required further optimisation and no definitive results were obtained from this analysis to date. However, the analysis of dendritic morphology of Purkinje cells was successful, which showed a "loss of self-avoidance" in the dendrites of Smchd1MommeD1/MommeD1 compared to Smchd1+/+ Purkinje cells. The restricted expression pattern of PCDHA isoforms was not altered to any great extent after knockdown or knockout of SMCHD1 (in combination with the loss of some DNA methylation) in human neuroblastoma cell lines SK-N-SH and SH-SH5Y. This finding indicates that once the pattern of PCDHA isoform expression has been chosen and epigenetically stabilised in the presence of SMCHD1, the subsequent loss of SMCHD1 is not sufficient to totally disrupt the pattern, even in combination with the loss of DNA methylation.

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Sun, Wei [Verfasser]. "RNA isoform analyses of Drosophila Dscam gene and Xenopus tropicalis clustered Protocadherin genes provide insights for neuronal self-avoidance / Wei Sun." Berlin : Freie Universität Berlin, 2016. http://d-nb.info/1098185358/34.

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Gallerani, Nicholas Edmund. "The spatial distribution of cortical interneurons: the role of clustered protocadherins." Thesis, 2021. https://doi.org/10.7916/d8-nbyk-3y33.

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The spatial patterning of neurons is a fundamental problem in neuroscience. The functions of the brain are rooted in the cellular architecture that underlies the structure of the brain. In the cerebral cortex, the functions of the cortex depend on the proper assembly of circuits made up of long-range excitatory neurons and locally-projecting inhibitory interneurons. Interneurons are incredibly diverse from a morphological and functional perspective and are found in every cortical area. Unlike excitatory cortical neurons, interneurons are born outside of the cortex and migrate long distances into the cortex and distribute across the cortex broadly. How do these diverse cells that essentially invade the cortex properly distribute? How do different developmental stages contribute to the final patterning of interneuron subtypes, and what are the molecules that influence this process? In this dissertation, I will present my original research which has advanced our knowledge of the answers to these fundamental questions in the field of developmental neuroscience. I addressed these questions by applying a range of techniques including mouse genetics, immunohistochemistry, confocal microscopy, and point pattern analysis. My research has shown that cortical interneuron subtypes are spatially independent. Spatial patterns of cortical interneuron subtypes are non-random within subtypes, but are randomly positioned with respect to other subtypes. I also explored the effects of loss of diversity within the clustered protocadherin family of adhesion molecules. Though these molecules do not appear to play a role in subtype specific spatial independence, I found that loss of clustered protocadherin diversity alters the density and laminar distribution of cortical interneuron subtypes. I also contributed to the development of genetic tools which could help us further understand how developmental stages contribute to final interneuron distribution. My original research has collectively advanced our knowledge of how cortical interneurons achieve their final distributions during development and has opened up new avenues of scientific inquiry for future research in developmental neuroscience.

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Mountoufaris, George. "The Role of the Clustered Protocadherins in the Assembly of Olfactory Neural Circuits." Thesis, 2016. https://doi.org/10.7916/D89K4BBT.

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The clustered protocadherins (Pcdh α, β & γ) provide individual neurons with cell surface diversity. However, the importance of Pcdh mediated diversity in neural circuit assembly and how it may promote neuronal connectivity remains largely unknown. Moreover, to date, Pcdh in vivo function has been studied at the level of individual gene clusters; whole cluster-wide function has not been addressed. Here I examine the role of all three Pcdh gene clusters in olfactory sensory neurons (OSNs); a neuronal type that expressed all three types of Pcdhs and in addition I address the role of Pcdh mediate diversity in their wiring. When OSNs share a dominant single Pcdh identity (α, β & γ) their axons fail to form distinct glomeruli, suggestive of inappropriate self-recognition of neighboring axons (loss of non-self-discrimination). By contrast, deletion of the entire α, β,γ Pcdh gene cluster, but not of each individual cluster alone, leads to loss of self-recognition and self-avoidance thus, OSN axons fail to properly arborize. I conclude that Pcdh-expression is necessary for self-recognition in OSNs, whereas its diversity allows distinction between self and non-self. Both of these functions are required for OSNs to connect and assembly into functional circuits in the olfactory bulb. My results, also reveal neuron-type specific differences in the requirement of specific Pcdh gene clusters and demonstrate significant redundancy between Pcdh isoforms in the olfactory system.

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8

Garcia, Sarah Theresa Kerfoot Myers Richard Barsh Gregory Stefan Brunet Anne Stearns Tim. "Genomic and regulatory network diversity revealed by REST/NRSF, maltase glucoamylase and the protocadherin gene cluster." 2010. http://purl.stanford.edu/mn338zt6208.

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Books on the topic "Clustered protocadherins"

1

Gallerani, Nicholas Edmund. The spatial distribution of cortical interneurons: The role of clustered protocadherins. [publisher not identified], 2021.

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2

Mountoufaris, George. The Role of the Clustered Protocadherins in the Assembly of Olfactory Neural Circuits. [publisher not identified], 2016.

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Book chapters on the topic "Clustered protocadherins"

1

Mah, Kar Men, and Joshua A. Weiner. "Clustered Protocadherins." In The Cadherin Superfamily. Springer Japan, 2016. http://dx.doi.org/10.1007/978-4-431-56033-3_8.

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2

Hirayama, Teruyoshi, and Takeshi Yagi. "Clustered Protocadherins and Neuronal Diversity." In Progress in Molecular Biology and Translational Science. Elsevier, 2013. http://dx.doi.org/10.1016/b978-0-12-394311-8.00007-8.

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3

McLeod, Cathy M., and Andrew M. Garrett. "Mouse models for the study of clustered protocadherins." In Current Topics in Developmental Biology. Elsevier, 2022. http://dx.doi.org/10.1016/bs.ctdb.2021.12.006.

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4

Yagi, Takeshi. "Role of the Clustered Protocadherins in Promoting Neuronal Diversity and Function." In Neural Surface Antigens. Elsevier, 2015. http://dx.doi.org/10.1016/b978-0-12-800781-5.00012-8.

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