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Academic literature on the topic 'CLN6'

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Published: 14 March 2023

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Journal articles on the topic "CLN6"

1

Levine, K., K. Huang, and F. R. Cross. "Saccharomyces cerevisiae G1 cyclins differ in their intrinsic functional specificities." Molecular and Cellular Biology 16, no. 12 (December 1996): 6794–803. http://dx.doi.org/10.1128/mcb.16.12.6794.

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The three budding yeast CLN genes appear to be functionally redundant for cell cycle Start: any single CLN gene is sufficient to promote Start, while the cln1 cln2 cln3 triple mutant is Start defective and inviable. Both quantitative and apparently qualitative differences between CLN genes have been reported, but available data do not in general allow distinction between qualitative functional differences as opposed to simply quantitative differences in expression or function. To determine if there are intrinsic qualitative differences between Cln proteins, we compared CLN2, CLN3, and crippled (but still partially active) CLN2 genes in a range of assays that differentiate genetically between CLN2 and CLN3. The results suggest that different potencies of Cln2, Cln3, and Cln2 mutants in functional assays cannot be accounted for by a simple quantitative model for their action, since Cln3 is at least as active as Cln2 and much more active than the Cln2 mutants in driving Swi4/Swi6 cell cycle box (SCB)-regulated transcription and cell cycle initiation in cln1 cln2 cln3 bck2 strains, but Cln3 has little or no activity in other assays in which Cln2 and the Cln2 mutants function. Differences in Cln protein abundance are unlikely to account for these results. Cln3-associated kinase is therefore likely to have an intrinsic in vivo substrate specificity distinct from that of Cln2-associated kinase, despite their functional redundancy. Consistent with the idea that Cln3 may be the primary transcriptional activator of CLN1, CLN2, and other genes, the activation of CLN2 transcription was found to be sensitive to the gene dosage of CLN3 but not to the gene dosage of CLN2.
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Epstein, C. B., and F. R. Cross. "Genes that can bypass the CLN requirement for Saccharomyces cerevisiae cell cycle START." Molecular and Cellular Biology 14, no. 3 (March 1994): 2041–47. http://dx.doi.org/10.1128/mcb.14.3.2041-2047.1994.

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Cell cycle START in Saccharomyces cerevisiae requires at least one of the three CLN genes (CLN1, CLN2, or CLN3). A total of 12 mutations bypassing this requirement were found to be dominant mutations in a single gene that we named BYC1 (for bypass of CLN requirement). We also isolated a plasmid that had cln bypass activity at a low copy number; the gene responsible was distinct from BYC1 and was identical to the recently described BCK2 gene. Strains carrying bck2::ARG4 disruption alleles were fully viable, but bck2::ARG4 completely suppressed the cln bypass activity of BYC1. swi4 and swi6 deletion alleles also efficiently suppressed BYC1 cln bypass activity; Swi4 and Swi6 are components of a transcription factor previously implicated in control of CLN1 and CLN2 expression. bck2::ARG4 was synthetically lethal with cln3 deletion, suggesting that CLN1 and CLN2 cannot function in the simultaneous absence of BCK2 and CLN3; this observation correlates with low expression of CLN1 and CLN2 in bck2 strains deprived of CLN3 function. Thus, factors implicated in CLN1 and CLN2 expression and/or function are also required for BYC1 function in the absence of all three CLN genes; this may suggest the involvement of other targets of Swi4, Swi6, and Bck2 in START.
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Epstein, C. B., and F. R. Cross. "Genes that can bypass the CLN requirement for Saccharomyces cerevisiae cell cycle START." Molecular and Cellular Biology 14, no. 3 (March 1994): 2041–47. http://dx.doi.org/10.1128/mcb.14.3.2041.

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Cell cycle START in Saccharomyces cerevisiae requires at least one of the three CLN genes (CLN1, CLN2, or CLN3). A total of 12 mutations bypassing this requirement were found to be dominant mutations in a single gene that we named BYC1 (for bypass of CLN requirement). We also isolated a plasmid that had cln bypass activity at a low copy number; the gene responsible was distinct from BYC1 and was identical to the recently described BCK2 gene. Strains carrying bck2::ARG4 disruption alleles were fully viable, but bck2::ARG4 completely suppressed the cln bypass activity of BYC1. swi4 and swi6 deletion alleles also efficiently suppressed BYC1 cln bypass activity; Swi4 and Swi6 are components of a transcription factor previously implicated in control of CLN1 and CLN2 expression. bck2::ARG4 was synthetically lethal with cln3 deletion, suggesting that CLN1 and CLN2 cannot function in the simultaneous absence of BCK2 and CLN3; this observation correlates with low expression of CLN1 and CLN2 in bck2 strains deprived of CLN3 function. Thus, factors implicated in CLN1 and CLN2 expression and/or function are also required for BYC1 function in the absence of all three CLN genes; this may suggest the involvement of other targets of Swi4, Swi6, and Bck2 in START.
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Vallen, E. A., and F. R. Cross. "Mutations in RAD27 define a potential link between G1 cyclins and DNA replication." Molecular and Cellular Biology 15, no. 8 (August 1995): 4291–302. http://dx.doi.org/10.1128/mcb.15.8.4291.

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The yeast Saccharomyces cerevisiae has three G1 cyclin (CLN) genes with overlapping functions. To analyze the functions of the various CLN genes, we examined mutations that result in lethality in conjunction with loss of cln1 and cln2. We have isolated alleles of RAD27/ERC11/YKL510, the yeast homolog of the gene encoding flap endonuclease 1, FEN-1.cln1 cln2 rad27/erc11 cells arrest in S phase; this cell cycle arrest is suppressed by the expression of CLN1 or CLN2 but not by that of CLN3 or the hyperactive CLN3-2. rad27/erc11 mutants are also defective in DNA damage repair, as determined by their increased sensitivity to a DNA-damaging agent, increased mitotic recombination rates, and increased spontaneous mutation rates. Unlike the block in cell cycle progression, these phenotypes are not suppressed by CLN1 or CLN2. CLN1 and CLN2 may activate an RAD27/ERC11-independent pathway specific for DNA synthesis that CLN3 is incapable of activating. Alternatively, CLN1 and CLN2 may be capable of overriding a checkpoint response which otherwise causes cln1 cln2 rad27/erc11 cells to arrest. These results imply that CLN1 and CLN2 have a role in the regulation of DNA replication. Consistent with this, GAL-CLN1 expression in checkpoint-deficient, mec1-1 mutant cells results in both cell death and increased chromosome loss among survivors, suggesting that CLN1 overexpression either activates defective DNA replication or leads to insensitivity to DNA damage.
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Cross, F. R. "Cell cycle arrest caused by CLN gene deficiency in Saccharomyces cerevisiae resembles START-I arrest and is independent of the mating-pheromone signalling pathway." Molecular and Cellular Biology 10, no. 12 (December 1990): 6482–90. http://dx.doi.org/10.1128/mcb.10.12.6482-6490.1990.

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Null mutations in three genes encoding cyclin-like proteins (CLN1, CLN2, and CLN3) in Saccharomyces cerevisiae cause cell cycle arrest in G1 (cln arrest). In cln1 cln2 cln3 strains bearing plasmids containing the CLN3 (also called WHI1 or DAF1) coding sequence under the transcriptional control of a galactose-regulated promoter, shift from galactose to glucose medium (shutting off synthesis of CLN3 mRNA) allowed completion of cell cycles in progress but caused arrest in the ensuing unbudded G1 phase. Cell growth was not inhibited in arrested cells. Cell division occurred in glucose medium even if cells were arrested in S phase during the initial 2 h of glucose treatment, suggesting that CLN function may not be required in the cell cycle after S phase. However, when the coding sequence of the hyperactive C-terminal truncation allele CLN3-2 (formerly DAF1-1) was placed under GAL control, cells went through multiple cycles before arresting after a shift from galactose to glucose. These results suggest that the C terminus of the wild-type protein confers functional instability. cln-arrested cells are mating competent. However, cln arrest is distinct from constitutive activation of the mating-factor signalling pathway because cln-arrested cells were dependent on the addition of pheromone both for mating and for induction of an alpha-factor-induced transcript, FUS1, and because MATa/MAT alpha (pheromone-nonresponsive) strains were capable of cln arrest in G1 (although a residual capacity for cell division before arrest was observed in MATa/MAT alpha strains). These results are consistent with a specific CLN requirement for START transit.
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Cross, F. R. "Cell cycle arrest caused by CLN gene deficiency in Saccharomyces cerevisiae resembles START-I arrest and is independent of the mating-pheromone signalling pathway." Molecular and Cellular Biology 10, no. 12 (December 1990): 6482–90. http://dx.doi.org/10.1128/mcb.10.12.6482.

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Null mutations in three genes encoding cyclin-like proteins (CLN1, CLN2, and CLN3) in Saccharomyces cerevisiae cause cell cycle arrest in G1 (cln arrest). In cln1 cln2 cln3 strains bearing plasmids containing the CLN3 (also called WHI1 or DAF1) coding sequence under the transcriptional control of a galactose-regulated promoter, shift from galactose to glucose medium (shutting off synthesis of CLN3 mRNA) allowed completion of cell cycles in progress but caused arrest in the ensuing unbudded G1 phase. Cell growth was not inhibited in arrested cells. Cell division occurred in glucose medium even if cells were arrested in S phase during the initial 2 h of glucose treatment, suggesting that CLN function may not be required in the cell cycle after S phase. However, when the coding sequence of the hyperactive C-terminal truncation allele CLN3-2 (formerly DAF1-1) was placed under GAL control, cells went through multiple cycles before arresting after a shift from galactose to glucose. These results suggest that the C terminus of the wild-type protein confers functional instability. cln-arrested cells are mating competent. However, cln arrest is distinct from constitutive activation of the mating-factor signalling pathway because cln-arrested cells were dependent on the addition of pheromone both for mating and for induction of an alpha-factor-induced transcript, FUS1, and because MATa/MAT alpha (pheromone-nonresponsive) strains were capable of cln arrest in G1 (although a residual capacity for cell division before arrest was observed in MATa/MAT alpha strains). These results are consistent with a specific CLN requirement for START transit.
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Jeoung, Doo-Il, L. J. W. M. Oehlen, and Frederick R. Cross. "Cln3-Associated Kinase Activity inSaccharomyces cerevisiae Is Regulated by the Mating Factor Pathway." Molecular and Cellular Biology 18, no. 1 (January 1, 1998): 433–41. http://dx.doi.org/10.1128/mcb.18.1.433.

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ABSTRACT The Saccharomyces cerevisiae cell cycle is arrested in G1 phase by the mating factor pathway. Genetic evidence has suggested that the G1 cyclins Cln1, Cln2, and Cln3 are targets of this pathway whose inhibition results in G1 arrest. Inhibition of Cln1- and Cln2-associated kinase activity by the mating factor pathway acting through Far1 has been described. Here we report that Cln3-associated kinase activity is inhibited by mating factor treatment, with dose response and timing consistent with involvement in cell cycle arrest. No regulation of Cln3-associated kinase was observed in a fus3 kss1 strain deficient in mating factor pathway mitogen-activated protein (MAP) kinases. Inhibition occurs mainly at the level of specific activity of Cln3-Cdc28 complexes. Inhibition of the C-terminally truncated Cln3-1-associated kinase is not observed; such truncations were previously identified genetically as causing resistance to mating factor-induced cell cycle arrest. Regulation of Cln3-associated kinase specific activity by mating factor treatment requires Far1. Overexpression of Far1 restores inhibition of C-terminally truncated Cln3-1-associated kinase activity. G2/M-arrested cells are unable to regulate Cln3-associated kinase, possibly because of cell cycle regulation of Far1 abundance. Inhibition of Cln3-associated kinase activity by the mating factor pathway may allow this pathway to block the earliest step in normal cell cycle initiation, since Cln3 functions as the most upstream G1-acting cyclin, activating transcription of the G1 cyclins CLN1 and CLN2 as well as of the S-phase cyclins CLB5 and CLB6.
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Vesa, Jouni, Mark H. Chin, Kathrin Oelgeschläger, Juha Isosomppi, Esteban C. DellAngelica, Anu Jalanko, and Leena Peltonen. "Neuronal Ceroid Lipofuscinoses Are Connected at Molecular Level: Interaction of CLN5 Protein with CLN2 and CLN3." Molecular Biology of the Cell 13, no. 7 (July 2002): 2410–20. http://dx.doi.org/10.1091/mbc.e02-01-0031.

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Neuronal ceroid lipofuscinoses (NCLs) are neurodegenerative storage diseases characterized by mental retardation, visual failure, and brain atrophy as well as accumulation of storage material in multiple cell types. The diseases are caused by mutations in the ubiquitously expressed genes, of which six are known. Herein, we report that three NCL disease forms with similar tissue pathology are connected at the molecular level: CLN5 polypeptides directly interact with the CLN2 and CLN3 proteins based on coimmunoprecipitation and in vitro binding assays. Furthermore, disease mutations in CLN5 abolished interaction with CLN2, while not affecting association with CLN3. The molecular characterization of CLN5 revealed that it was synthesized as four precursor forms, due to usage of alternative initiator methionines in translation. All forms were targeted to lysosomes and the longest form, translated from the first potential methionine, was associated with membranes. Interactions between CLN polypeptides were shown to occur with this longest, membrane-bound form of CLN5. Both intracellular targeting and posttranslational glycosylation of the polypeptides carrying human disease mutations were similar to wild-type CLN5.
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Di Como, C. J., H. Chang, and K. T. Arndt. "Activation of CLN1 and CLN2 G1 cyclin gene expression by BCK2." Molecular and Cellular Biology 15, no. 4 (April 1995): 1835–46. http://dx.doi.org/10.1128/mcb.15.4.1835.

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The Saccharomyces cerevisiae CLN3 protein, a G1 cyclin, positively regulates the expression of CLN1 and CLN2, two additional G1 cyclins whose expression during late G1 is activated, in part, by the transcription factors SWI4 and SWI6. We isolated 12 complementation groups of mutants that require CLN3. The members of one of these complementation groups have mutations in the BCK2 gene. In a wild-type CLN3 genetic background, bck2 mutants have a normal growth rate but have a larger cell size, are more sensitive to alpha-factor, and have a modest defect in the accumulation of CLN1 and CLN2 RNA. In the absence of CLN3, bck2 mutations cause an extremely slow growth rate: the cells accumulate in late G1 with very low levels of CLN1 and CLN2 RNA. The slow growth rate and long G1 delay of bck2 cln3 mutants are cured by heterologous expression of CLN2. Moreover, overexpression of BCK2 induces very high levels of CLN1, CLN2, and HCS26 RNAs. The results suggest that BCK2 and CLN3 provide parallel activation pathways for the expression of CLN1 and CLN2 during late G1.
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HEINE, Claudia, Jaana TYYNELÄ, Jonathan D. COOPER, David N. PALMER, Milan ELLEDER, Alfried KOHLSCHÜTTER, and Thomas BRAULKE. "Enhanced expression of manganese-dependent superoxide dismutase in human and sheep CLN6 tissues." Biochemical Journal 376, no. 2 (December 1, 2003): 369–76. http://dx.doi.org/10.1042/bj20030598.

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Neuronal ceroid lipofuscinosis type 6 and its sheep model (OCL6) are lysosomal storage disorders caused by mutations in the CLN6 gene product of unknown function. It has been proposed that mitochondrial dysfunction, including defects in mitochondrial protein degradation, organelle enlargement and functional changes in oxidative phosphorylation, may contribute to the disease pathology. To further explore the disease mechanisms underlying CLN6, protein expression was compared between normal and affected tissues. Using two-dimensional electrophoretic separation of proteins, MS and immunoblotting, MnSOD (manganese-dependent superoxide dismutase) was found to be significantly and specifically increased in fibroblasts and brain extracts of both human and sheep affected with CLN6. Both the activity and expression of MnSOD mRNA were enhanced in affected fibroblasts. Confocal fluorescence microscopy and immunohistochemical studies revealed the presence of MnSOD in mitochondria of CLN6 fibroblasts and in CLN6 brain sections within both neurons and hypertrophic astrocytes. These data suggest that oxidative stress and/or the production of pro-inflammatory cytokines are characteristic features of human and sheep CLN6, resulting in elevated expression of MnSOD, which may be important for diagnostic purposes.
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Dissertations / Theses on the topic "CLN6"

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Martin, Yella. "Investigation of the Batten Disease protein CLN6." Thesis, University College London (University of London), 2006. http://discovery.ucl.ac.uk/1444803/.

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The neuronal ceroid lipofuscinoses (NCLs, Batten Disease) are a group of lysosomal storage disorders caused by mutations in known and unknown proteins with different cellular locations. Mutations in the CLN6 gene cause a type of variant late infantile NCL (vLINCL). The CLN6 protein is located in the ER and how mutations in CLN6 cause accumulation of storage material in the lysosome is unclear. The aims of this thesis were to establish the tools and techniques necessary to analyse the CLN6 protein and to utilise these to investigate its subcellular location, to identify proteins that interact with CLN6 and to elucidate the early cellular responses to loss of functional vLINCL proteins, CLN5, CLN6 and CLN8. It was shown that CLN6 can be detected by Western blotting, indirect immunofluorescence and immunoprecipitation. A construct of CLN6 fused to horseradish peroxidase was cloned for localisation studies by indirect immunofluorescence and electron microscopy. CLN6 protein and mRNA levels could be depleted using RNA interference and this depletion assessed by Western blotting, indirect immunofluorescence and Q-PCR. It was not possible to establish whether CLN6 is located within a sub-domain of the ER using indirect immunofluorescence or electron microscopy. There was no effect on the localisation or stabilisation of wild-type or mutant CLN6 when proteasomal or lysosomal inhibitors were used, indicating that CLN6 does not traffic to the lysosome and that wild-type and mutant CLN6 were not degraded by ER-associated degradation. Endogenous CLN6 was identified in co-immunoprecipitation experiments, confirming that it may bind to itself. No other proteins were identified that bind to CLN6. Depletion of CLN5, CLN6 and CLN8 resulted in an increase in the size and a redistribution to perinuclear areas of late endosomes and lysosomes. An increase in long cis-Go g structures was also observed in response to siRNA against CLN6 and CLN8 but not CLN5.
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Mohd, Ismail Izmira Farhana. "Identification of a novel mutation in the CLN6 gene (CLN6) in South Hampshire sheep affected with Neuronal Ceroid Lipofuscinosis." Thesis, The University of Sydney, 2014. http://hdl.handle.net/2123/14579.

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Neuronal ceroid lipofuscinoses (NCL/Batten disease) are a group of fatal inherited neurodegenerative diseases that occur in many species including humans, sheep, dogs and cattle. Typical NCL symptoms include progressive loss of vision, regression of mental and motor development, epileptic seizures and premature death. Currently there is no effective treatment or cure for NCL, with the underlying disease mechanisms still poorly understood. Advances in molecular genetics in recent years have allowed the characterisation of hundreds of causative mutations and polymorphisms in at least 17 disease-causing genes across all species. For some species, research colonies have been established for studies relevant to the corresponding human NCL variants. Best characterised of all animal models for NCL is the New Zealand South Hampshire (SH) sheep which is a model for the human variant late-infantile form of NCL (vLINCL). Past studies have revealed the ovine CLN6 gene (CLN6) as a strong candidate gene for this disease in South Hampshire sheep however no disease-causing mutation was identified. The main objective of the present thesis is the identification and characterisation of the mutation responsible for NCL in the South Hampshire sheep. It was proposed that the mutation lies in the non-coding regions within or flanking the gene and that this mutation affects gene regulation. Bioinformatic tools were initially used to identify conserved non-coding sequences (CNCS) which are deemed potential regions of interest for regulatory mutations. Due to the limited ovine genome resource available when the study was commenced in 2006, CLN6 orthologous sequences from other species were initially used for identification of highly conserved regions. Of the five identified CNCS (5’ UTR, 3’UTR and introns 1, 2 and 6) the region upstream of CLN6 and intron 1 were considered priorities for sequencing. Given that the Sanger sequencing method was laborious and time-consuming, and that there was rapid development of technology; the Sanger sequencing approach was abandoned and Next-generation sequencing (NGS) methods utilised for the following studies. The 454 Pyrosequencing NGS technology was used to sequence the complete ovine Bacterial artificial chromosome (BAC) to generate an ovine reference sequence for mutation screening approaches. The first mutation screening approach, sequence capture and targeted sequencing approach failed; however, the second approach involving sequencing of long-range PCR (LR-PCR) products successfully identified the disease-causing mutation. LR-PCR amplification of 14 regions within the ovine genome region spanning the CLN6 and flanking sequences followed by SOLID sequencing-by-ligation NGS method identified the disease-associated mutation as a 402bp deletion and 1bp insertion in ovine CLN6, namely g.-251_+150del and g.+150_151insC. The mutation is predicted to lead to the deletion of the whole of exon 1 and the ATG start codon as well as flanking non-coding sequence. Identifying the disease-causing mutation for NCL in SH sheep provides the long-awaited confirmatory evidence that ovine CLN6 is the causative gene for NCL in SH sheep. Future research in this large animal model will allow for more effective strategies for developing therapeutic approaches for NCL in humans and further strengthens the invaluable role of this animal model for NCL studies.
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Cramer, Thomas [Verfasser]. "Generierung monoklonaler Antikörper gegen das Protein CLN6 / Thomas Cramer." Halle, 2017. http://d-nb.info/118038783X/34.

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Alves, Mariana Isabel Quaresma da Rocha. "Ceroido-Lipofuscinose Neuronal. Estudos de localização celular da proteína CLN6." Master's thesis, Faculdade de Medicina da Universidade do Porto, 2007. http://hdl.handle.net/10216/22151.

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Alves, Mariana Isabel Quaresma da Rocha. "Ceroido-Lipofuscinose Neuronal. Estudos de localização celular da proteína CLN6." Dissertação, Faculdade de Medicina da Universidade do Porto, 2007. http://hdl.handle.net/10216/22151.

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Dahlmann, Cordula [Verfasser]. "Retinaler Phänotyp dreier Mausmodelle für die neuronale Ceroidlipofuszinose : (CLN1-knockout Mausmodell, CLN3Δex7/8-knock-in Mausmodell und CLN6-knockout Mausmodell) / Cordula Dahlmann." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2013. http://d-nb.info/1031097074/34.

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Lauronen, Leena. "Neuromagnetic studies on somatosensory functions in CLN3, CLN5 and CLN8 forms of neuronal ceroid lipofuscinoses." Helsinki : University of Helsinki, 2001. http://ethesis.helsinki.fi/julkaisut/laa/kliin/vk/lauronenle/.

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Trusso, Maria Allegra. "THE GENETICS OF BIPOLAR DISORDER AND THE ROLE OF HETEROZYGOSITY FOR NEURONAL CEROID LIPOFUSCINOSIS." Doctoral thesis, Università di Siena, 2022. http://hdl.handle.net/11365/1214195.

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Introduction. Bipolar Disorder (BD) is an heritable chronic mental disorder causing psychosocial impairment, affecting patients with depressive/manic episodes. The familial transmission of BD does not follow any of the simple Mendelian patterns of inheritance, demonstrating the involvement of multiple susceptibility genes. Materials and Method. Whole Exome Sequencing (WES) was performed in eight subjects of a large family counting twelve BD affected people. We selected variants in common between the affected subjects, once including and once excluding a “borderline” subject with moderate anxiety and traits of obsessive- compulsive disorder.  Results. Results were in favour of a Digenic model of transmission, with a heterozygous missense variant in CLN6 resulting in a “borderline” phenotype that if combined with a heterozygous missense variant in ZNF92 is responsible for the more severe BD phenotype. Both rare missense changes are predicted to disrupt the protein function. Conclusions. Loss of both alleles in CLN6 causes Neuronal Ceroid Lipofuscinosis, a severe progressive neurological disorder of childhood. Our results indicate that heterozygous CLN6 carriers, previously reported as healthy, may be susceptible to bipolar disorder late in life. Additional variants, such as that in ZNF92 reported here, may further worsen the phenotype in a setting of digenic disorder. Further investigation on a larger cohort should be performed in order to better characterize the contribution of each gene.
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Krzoska, Marta [Verfasser], and Thomas [Akademischer Betreuer] Braulke. "Untersuchungen zur Interaktion des krankheitsrelevanten CLN6-Proteins mit der Inositollipidphosphatase TPIP / Marta Krzoska. Betreuer: Thomas Braulke." Hamburg : Staats- und Universitätsbibliothek Hamburg, 2011. http://d-nb.info/1020384301/34.

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Bessa, Carlos Jorge Pereira. "Molecular pathophysiology underlyng neuronal ceroid lipofuscinoses: CLN2 and CLN5." Doctoral thesis, Instituto de Ciências Biomédicas Abel Salazar, 2009. http://hdl.handle.net/10216/24457.

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Books on the topic "CLN6"

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National Alliance of Certified Legal Nurse Consultants. Conference. Discover your natural edge for CLNC success. Houston, TX (5615 Kirby Dr., Houston 77005-2448): Vickie Milazzo Institute, 2006.

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Milazzo, Vickie L. CLNC Certified Legal Nurse Consultant success stories: Real nurses, real stories, unreal success. Edited by Medical-Legal Consulting Institute. 4th ed. Houston, Tex: Vickie Milazzo Institute, a division of the Medical-Legal Consulting Institute, Inc., 2008.

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1924-, De Simone Pasquale, ed. La Vana battaglia per il plebiscito. [Gorizia]: Anvgd Gorizia, 1990.

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Create your own magic for CLNC success: A unique book of 91 devilishly practical potions. 2nd ed. Houston, Tex: Vickie Milazzo Institute, 2008.

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National Alliance of Certified Legal Nurse Consultants. Conference. Build your bridge to CLNC gold: National Alliance of Certified Legal Nurse Consultants Ninth Annual Conference. Houston, TX (2476 Bolsover St., Houston 77005): Vickie Milazzo Institute, 2004.

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Delord, J. La langue kabj̳ye̳ et ses divers aspects: Correspondance avec le Comité de langue nationale kabj̳ye̳ (CLNK). [Lomé]: Éditions HAHO, 2000.

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Ferruccio, Vendramini, and Borghi Marco, eds. I CLN di Belluno e Treviso nella lotta di liberazione: Atti e documenti. Padova: Istituto veneto per la storia della Resistenza e dell'età contemporanea, 1999.

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Conference, National Alliance of Certified Legal Nurse Consultants. Go all in for sensational CLNC success: National Alliance of Certified Legal Nurse Consultants Thirteenth Annual Conference. Houston, TX: Vickie Milazzo Institute/National Alliance of Certified Legal Nurse Consultants, 2008.

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National Alliance of Certified Legal Nurse Consultants. Conference. CLNC magic: The sweet spell of success : National Alliance of Certified Legal Nurse Consultants Eighth Annual Conference. Houston, TX (2476 Bolsover St., Houston, 77005): Vickie Milazzo Institute, 2003.

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J, Lee Timothy, and United States. National Aeronautics and Space Administration., eds. Accurate ab initio quartic force fields, vibrational frequencies, and heats of formation for FCN, FNC, ClCN, and ClNC. [Washington, DC: National Aeronautics and Space Administration, 1995.

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Book chapters on the topic "CLN6"

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Zahid, Sarwar, Kari Branham, Dana Schlegel, Mark E. Pennesi, Michel Michaelides, John Heckenlively, and Thiran Jayasundera. "CLN3." In Retinal Dystrophy Gene Atlas, 59–60. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-10867-4_18.

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Herber, R. H., and B. J. Masters. "Chlorine(Cl36 )-Labeled Deuterium Chloride: [Hydrogen-D Chloride (Cl36 )]." In Inorganic Syntheses, 155–60. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2007. http://dx.doi.org/10.1002/9780470132388.ch43.

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Hirota, E., K. Kuchitsu, T. Steimle, J. Vogt, and N. Vogt. "83 ClNO Nitrosyl chloride." In Molecules Containing No Carbon Atoms and Molecules Containing One or Two Carbon Atoms, 114. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-540-70614-4_84.

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Hirota, E., K. Kuchitsu, T. Steimle, J. Vogt, and N. Vogt. "85 ClN3 Chlorine azide." In Molecules Containing No Carbon Atoms and Molecules Containing One or Two Carbon Atoms, 116. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-540-70614-4_86.

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Jain, M., and A. Gupta. "2480 Diamagnetic susceptibility of ClNa." In Diamagnetic Susceptibility and Anisotropy of Inorganic and Organometallic Compounds, 2530. Berlin, Heidelberg: Springer Berlin Heidelberg, 2007. http://dx.doi.org/10.1007/978-3-540-44694-1_2481.

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Villars, P., K. Cenzual, J. Daams, R. Gladyshevskii, O. Shcherban, V. Dubenskyy, N. Melnichenko-Koblyuk, et al. "[NH4]4Ir[NO3]Cl6." In Landolt-Börnstein - Group III Condensed Matter, 734. Berlin, Heidelberg: Springer Berlin Heidelberg, 2008. http://dx.doi.org/10.1007/978-3-540-44752-8_620.

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Hüttner, W. "183 ClNa X 1Σ+ Sodium chloride." In Diamagnetic Diatomic Molecules. Part 1, 253–54. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-540-69954-5_185.

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Hüttner, W. "184 ClNb X 5П Niobium chloride." In Diamagnetic Diatomic Molecules. Part 1, 255. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-540-69954-5_186.

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Chihara, H., and N. Nakamura. "NQRS Data for ClNa(Subst. No. 1850)." In Substances Containing C10H16 … Zn, 708. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-642-02943-1_585.

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Chihara, H., and N. Nakamura. "NQRS Data for ClNa(Subst. No. 1851)." In Substances Containing C10H16 … Zn, 709. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-642-02943-1_586.

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Conference papers on the topic "CLN6"

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"Mutation c.396dupT in the CLN6 gene – the main cause of neuronal ceroid lipofucinosis in Yakutia." In Bioinformatics of Genome Regulation and Structure/Systems Biology (BGRS/SB-2022) :. Institute of Cytology and Genetics, the Siberian Branch of the Russian Academy of Sciences, 2022. http://dx.doi.org/10.18699/sbb-2022-228.

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Shanmugasundaram, Karthikeyan, S. Sharma, and Sathees Kumar Ramasamy. "Face recognition with CLNF for uncontrolled occlusion faces." In 2016 IEEE International Conference on Recent Trends in Electronics, Information & Communication Technology (RTEICT). IEEE, 2016. http://dx.doi.org/10.1109/rteict.2016.7808124.

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Wood, Stephen L., and Gisela S. Bahr. "Autonomous Sub-Surface Covert Littoral Node (CLN)." In OCEANS 2018 MTS/IEEE Charleston. IEEE, 2018. http://dx.doi.org/10.1109/oceans.2018.8604582.

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Liu, Li, Gang Feng, and Denis Beautemps. "Automatic dynamic template tracking of inner lips based on CLNF." In 2017 IEEE International Conference on Acoustics, Speech and Signal Processing (ICASSP). IEEE, 2017. http://dx.doi.org/10.1109/icassp.2017.7953134.

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Fontes, Ana L., Lígia L. Pimentel, Luis M. Rodríguez-Alcalá, and Ana M. Gomes. "Stability of a Fermented Milk Enriched With Microbial CLA/CLNA." In The 7th World Congress on New Technologies. Avestia Publishing, 2021. http://dx.doi.org/10.11159/icbb21.231.

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Albuquerque, Vitória, Ernesto Caffarena, and João Silva. "Computational design of neutralizing scfv for gastric cancer protein cldn6." In International Symposium on Immunobiologicals. Instituto de Tecnologia em Imunobiológicos, 2022. http://dx.doi.org/10.35259/isi.2022_52286.

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Plourde, M., P. Angers, and J. L. Sébédio. "Evaluation of the Physiological Effects of Conjugated Alpha-Linolenic Acids (CLnA)." In 13th World Congress of Food Science & Technology. Les Ulis, France: EDP Sciences, 2006. http://dx.doi.org/10.1051/iufost:20061371.

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Stafford, Lewis J., Brad Screnci, Chidananda Sulli, Erin Rosenberg, Nicholas Molino, David Tucker, Jonathan Sullivan, et al. "Abstract 5759: Discovery of a novel claudin 6 (CLDN6) specific monoclonal antibody." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-5759.

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Jiun-In, Guo, Tsai Chi-Chi, and Tseng Ching-Kan. "Pvalite CLN: Lightweight Object Detection with Classfication and Localization Network." In 2019 32nd IEEE International System-on-Chip Conference (SOCC). IEEE, 2019. http://dx.doi.org/10.1109/socc46988.2019.1570561207.

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Gioventu, Alessandra. "B-flavour anomalies in b->sll and b->clnu transitions at LHCb." In XXVII International Workshop on Deep-Inelastic Scattering and Related Subjects. Trieste, Italy: Sissa Medialab, 2019. http://dx.doi.org/10.22323/1.352.0252.

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Reports on the topic "CLN6"

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Marlow, D. Host Group Extensions for CLNP Multicasting. RFC Editor, March 1995. http://dx.doi.org/10.17487/rfc1768.

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Christian, P. Generic Routing Encapsulation over CLNS Networks. RFC Editor, July 2001. http://dx.doi.org/10.17487/rfc3147.

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Piscitello, D. Use of ISO CLNP in TUBA Environments. RFC Editor, December 1993. http://dx.doi.org/10.17487/rfc1561.

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Hares, S., and C. Wittbrodt. An Echo Function for CLNP (ISO 8473). RFC Editor, February 1994. http://dx.doi.org/10.17487/rfc1575.

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Piscitello, D. Assignment of System Identifiers for TUBA/CLNP Hosts. RFC Editor, September 1993. http://dx.doi.org/10.17487/rfc1526.

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Halpern, J. M. OSI CLNS and LLC1 protocols on Network Systems HYPERchannel. RFC Editor, May 1991. http://dx.doi.org/10.17487/rfc1223.

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Satz, G. CLNS MIB for use with Connectionless Network Protocol (ISO 8473) and End System to Intermediate System (ISO 9542). RFC Editor, June 1991. http://dx.doi.org/10.17487/rfc1238.

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