Готові списки джерел за темами / CRISPR-Ca

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Добірка наукової літератури з теми "CRISPR-Ca"

Автор: Grafiati

Опубліковано: 11 березня 2023

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Статті в журналах з теми "CRISPR-Ca"

Molina, Rafael, Anne Louise Grøn Jensen, Javier Marchena-Hurtado, Blanca López-Méndez, Stefano Stella, and Guillermo Montoya. "Structural basis of cyclic oligoadenylate degradation by ancillary Type III CRISPR-Cas ring nucleases." Nucleic Acids Research 49, no. 21 (November 26, 2021): 12577–90. http://dx.doi.org/10.1093/nar/gkab1130.

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Abstract Type III CRISPR-Cas effector systems detect foreign RNA triggering DNA and RNA cleavage and synthesizing cyclic oligoadenylate molecules (cA) in their Cas10 subunit. cAs act as a second messenger activating auxiliary nucleases, leading to an indiscriminate RNA degradation that can end in cell dormancy or death. Standalone ring nucleases are CRISPR ancillary proteins which downregulate the strong immune response of Type III systems by degrading cA. These enzymes contain a CRISPR-associated Rossman-fold (CARF) domain, which binds and cleaves the cA molecule. Here, we present the structures of the standalone ring nuclease from Sulfolobus islandicus (Sis) 0811 in its apo and post-catalytic states. This enzyme is composed by a N-terminal CARF and a C-terminal wHTH domain. Sis0811 presents a phosphodiester hydrolysis metal-independent mechanism, which cleaves cA4 rings to generate linear adenylate species, thus reducing the levels of the second messenger and switching off the cell antiviral state. The structural and biochemical analysis revealed the coupling of a cork-screw conformational change with the positioning of key catalytic residues to proceed with cA4 phosphodiester hydrolysis in a non-concerted manner.

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Starkuviene, Vytaute, Stefan M. Kallenberger, Nina Beil, Tautvydas Lisauskas, Bastian So-Song Schumacher, Ruben Bulkescher, Piotr Wajda, Manuel Gunkel, Jürgen Beneke, and Holger Erfle. "High-Density Cell Arrays for Genome-Scale Phenotypic Screening." SLAS DISCOVERY: Advancing the Science of Drug Discovery 24, no. 3 (January 25, 2019): 274–83. http://dx.doi.org/10.1177/2472555218818757.

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Due to high associated costs and considerable time investments of cell-based screening, there is a strong demand for new technologies that enable preclinical development and tests of diverse biologicals in a cost-saving and time-efficient manner. For those reasons we developed the high-density cell array (HD-CA) platform, which miniaturizes cell-based screening in the form of preprinted and ready-to-run screening arrays. With the HD-CA technology, up to 24,576 samples can be tested in a single experiment, thereby saving costs and time for microscopy-based screening by 75%. Experiments on the scale of the entire human genome can be addressed in a real parallel manner, with screening campaigns becoming more comfortable and devoid of robotics infrastructure on the user side. The high degree of miniaturization enables working with expensive reagents and rare and difficult-to-obtain cell lines. We have also optimized an automated imaging procedure for HD-CA and demonstrate the applicability of HD-CA to CRISPR-Cas9- and RNAi-mediated phenotypic assessment of the gene function.

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Lee, Ji Young, Mikhail Alexeyev, Natalya Kozhukhar, Viktoriya Pastukh, Roderica White, and Troy Stevens. "Carbonic anhydrase IX is a critical determinant of pulmonary microvascular endothelial cell pH regulation and angiogenesis during acidosis." American Journal of Physiology-Lung Cellular and Molecular Physiology 315, no. 1 (July 1, 2018): L41—L51. http://dx.doi.org/10.1152/ajplung.00446.2017.

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Carbonic anhydrase IX (CA IX) is highly expressed in rapidly proliferating and highly glycolytic cells, where it serves to enhance acid-regulatory capacity. Pulmonary microvascular endothelial cells (PMVECs) actively utilize aerobic glycolysis and acidify media, whereas pulmonary arterial endothelial cells (PAECs) primarily rely on oxidative phosphorylation and minimally change media pH. Therefore, we hypothesized that CA IX is critical to PMVEC angiogenesis because of its important role in regulating pH. To test this hypothesis, PMVECs and PAECs were isolated from Sprague-Dawley rats. CA IX knockout PMVECs were generated using the CRISPR-Cas9 technique. During serum-stimulated growth, mild acidosis (pH 6.8) did not affect cell counts of PMVECs, but it decreased PAEC cell number. Severe acidosis (pH 6.2) decreased cell counts of PMVECs and elicited an even more pronounced reduction of PAECs. PMVECs had a higher CA IX expression compared with PAECs. CA activity was higher in PMVECs compared with PAECs, and enzyme activity was dependent on the type IX isoform. Pharmacological inhibition and genetic ablation of CA IX caused profound dysregulation of extra- and intracellular pH in PMVECs. Matrigel assays revealed impaired angiogenesis of CA IX knockout PMVECs in acidosis. Lastly, pharmacological CA IX inhibition caused profound cell death in PMVECs, whereas genetic CA IX ablation had little effect on PMVEC cell death in acidosis. Thus CA IX controls PMVEC pH necessary for angiogenesis during acidosis. CA IX may contribute to lung vascular repair during acute lung injury that is accompanied by acidosis within the microenvironment.

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Wang, Longlong, Jianjun Liang, Yu Zhou, Tao Tian, Baoli Zhang, and Deqiang Duanmu. "Molecular Characterization of Carbonic Anhydrase Genes in Lotus japonicus and Their Potential Roles in Symbiotic Nitrogen Fixation." International Journal of Molecular Sciences 22, no. 15 (July 21, 2021): 7766. http://dx.doi.org/10.3390/ijms22157766.

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Carbonic anhydrase (CA) plays a vital role in photosynthetic tissues of higher plants, whereas its non-photosynthetic role in the symbiotic root nodule was rarely characterized. In this study, 13 CA genes were identified in the model legume Lotus japonicus by comparison with Arabidopsis CA genes. Using qPCR and promoter-reporter fusion methods, three previously identified nodule-enhanced CA genes (LjαCA2, LjαCA6, and LjβCA1) have been further characterized, which exhibit different spatiotemporal expression patterns during nodule development. LjαCA2 was expressed in the central infection zone of the mature nodule, including both infected and uninfected cells. LjαCA6 was restricted to the vascular bundle of the root and nodule. As for LjβCA1, it was expressed in most cell types of nodule primordia but only in peripheral cortical cells and uninfected cells of the mature nodule. Using CRISPR/Cas9 technology, the knockout of LjβCA1 or both LjαCA2 and its homolog, LjαCA1, did not result in abnormal symbiotic phenotype compared with the wild-type plants, suggesting that LjβCA1 or LjαCA1/2 are not essential for the nitrogen fixation under normal symbiotic conditions. Nevertheless, the nodule-enhanced expression patterns and the diverse distributions in different types of cells imply their potential functions during root nodule symbiosis, such as CO2 fixation, N assimilation, and pH regulation, which await further investigations.

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Liu, Xiaoyan, Yu Zhang, Su Wang, Guoying Liu, and Liming Ruan. "Loss of miR-143 and miR-145 in condyloma acuminatum promotes cellular proliferation and inhibits apoptosis by targeting NRAS." Royal Society Open Science 5, no. 8 (August 2018): 172376. http://dx.doi.org/10.1098/rsos.172376.

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The expression profile of miRNAs and their function in condyloma acuminatum (CA) remains unknown. In this study, we aimed to detect the effects of miR-143 and miR-145, the most downregulated in CA samples using high-throughput sequencing, on cell proliferation and apoptosis, to determine a novel therapeutic target for CA recurrence. RT-qPCR was used to validate the lower expression of miR-143 and miR-145 in a larger size of CA samples, and the expression of NRAS in CA samples was significantly higher than self-controls as determined by western blotting assay. Luciferase assay was performed to confirm that miR-143 or miR-145 targeted NRAS directly. Transduction of LV-pre-miR-143 or LV-pre-miR-145 to human papilloma virus (HPV)-infected SiHa cells led to reduced proliferation, greater apoptosis and inhibition of expression of NRAS, PI3 K p110 α and p-AKT. However, knockout of miR-143 or miR-145 in human epidermal keratinocytes by delivery of CRISPR/CAS9-gRNA for target miRNAs protected cells from apoptosis and upregulated expression of target genes as described above. MiR-143 and miR-145 sensitized cells to nutlin-3a, a p53 activator and MDM2 antagonist, while their loss protected cells from the stress of nutlin-3a. Furthermore, siRNA targeting NRAS showed similar effects on proliferation and apoptosis as miR-143 or miR-145. Taken together, our results suggest that loss of miR-143 or miR-145 in CA protects HPV-infected cells from apoptosis induced by environmental stress, in addition to promoting cellular proliferation and inhibiting apoptosis by targeting NRAS/PI3 K/ATK. Restoration of miR-143 or miR-145 might provide an applicable and novel approach to block the recurrence and progression of CA.

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Lee, Ji Young, Mher Onanyan, Ian Garrison, Roderica White, Maura Crook, Mikhail F. Alexeyev, Natalya Kozhukhar, et al. "Extrinsic acidosis suppresses glycolysis and migration while increasing network formation in pulmonary microvascular endothelial cells." American Journal of Physiology-Lung Cellular and Molecular Physiology 317, no. 2 (August 1, 2019): L188—L201. http://dx.doi.org/10.1152/ajplung.00544.2018.

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Acidosis is common among critically ill patients, but current approaches to correct pH do not improve disease outcomes. During systemic acidosis, cells are either passively exposed to extracellular acidosis that other cells have generated (extrinsic acidosis) or they are exposed to acid that they generate and export into the extracellular space (intrinsic acidosis). Although endothelial repair following intrinsic acidosis has been studied, the impact of extrinsic acidosis on migration and angiogenesis is unclear. We hypothesized that extrinsic acidosis inhibits metabolism and migration but promotes capillary-like network formation in pulmonary microvascular endothelial cells (PMVECs). Extrinsic acidosis was modeled by titrating media pH. Two types of intrinsic acidosis were compared, including increasing cellular metabolism by chemically inhibiting carbonic anhydrases (CAs) IX and XII (SLC-0111) and with hypoxia. PMVECs maintained baseline intracellular pH for 24 h with both extrinsic and intrinsic acidosis. Whole cell CA IX protein expression was decreased by extrinsic acidosis but not affected by hypoxia. When extracellular pH was equally acidic, extrinsic acidosis suppressed glycolysis, whereas intrinsic acidosis did not. Extrinsic acidosis suppressed migration, but increased Matrigel network master junction and total segment length. CRISPR-Cas9 CA IX knockout PMVECs revealed an independent role of CA IX in promoting glycolysis, as loss of CA IX alone was accompanied by decreased hexokinase I and pyruvate dehydrogenase E1α expression and decreasing migration. 2-deoxy-d-glucose had no effect on migration but profoundly inhibited network formation and increased N-cadherin expression. Thus, we report that while extrinsic acidosis suppresses endothelial glycolysis and migration, it promotes network formation.

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Averina, Olga A., M. Y. Vysokikh, O. A. Permyakov, and P. V. Sergiev. "Simple recommendations for improving efficiency in generating genome-edited mice." Acta Naturae 12, no. 1 (April 16, 2020): 42–50. http://dx.doi.org/10.32607/actanaturae.10937.

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The generation of transgenic model organisms (primarily mice) is an integral part of modern fundamental and applied research. Simple techniques based on the biology of these laboratory rodents can often increase efficiency when generating genome-edited mouse strains. In this study, we share our three years of experience in the optimization of mouse genome editing based on microinjection of CRISPR/Cas9 components into ca. 10,000 zygotes. We tested a number of techniques meant to improve efficiency in generating knockout mice, such as optimization of the superovulation method and choosing the optimal mouse strains to be used as zygote donors and foster mothers. The presented results might be useful to laboratories aiming to quickly and efficiently create new mouse strains with tailored genome editing.

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Campbell, Hannah M., Ann P. Quick, Issam Abu-Taha, David Y. Chiang, Carlos F. Kramm, Tarah A. Word, Sören Brandenburg, et al. "Loss of SPEG Inhibitory Phosphorylation of Ryanodine Receptor Type-2 Promotes Atrial Fibrillation." Circulation 142, no. 12 (September 22, 2020): 1159–72. http://dx.doi.org/10.1161/circulationaha.120.045791.

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Background: Enhanced diastolic calcium (Ca 2+ ) release through ryanodine receptor type-2 (RyR2) has been implicated in atrial fibrillation (AF) promotion. Diastolic sarcoplasmic reticulum Ca 2+ leak is caused by increased RyR2 phosphorylation by PKA (protein kinase A) or CaMKII (Ca 2+ /calmodulin-dependent kinase-II) phosphorylation, or less dephosphorylation by protein phosphatases. However, considerable controversy remains regarding the molecular mechanisms underlying altered RyR2 function in AF. We thus aimed to determine the role of SPEG (striated muscle preferentially expressed protein kinase), a novel regulator of RyR2 phosphorylation, in AF pathogenesis. Methods: Western blotting was performed with right atrial biopsies from patients with paroxysmal AF. SPEG atrial knockout mice were generated using adeno-associated virus 9. In mice, AF inducibility was determined using intracardiac programmed electric stimulation, and diastolic Ca 2+ leak in atrial cardiomyocytes was assessed using confocal Ca 2+ imaging. Phosphoproteomics studies and Western blotting were used to measure RyR2 phosphorylation. To test the effects of RyR2-S2367 phosphorylation, knockin mice with an inactivated S2367 phosphorylation site (S2367A) and a constitutively activated S2367 residue (S2367D) were generated by using CRISPR-Cas9. Results: Western blotting revealed decreased SPEG protein levels in atrial biopsies from patients with paroxysmal AF in comparison with patients in sinus rhythm. SPEG atrial-specific knockout mice exhibited increased susceptibility to pacing-induced AF by programmed electric stimulation and enhanced Ca 2+ spark frequency in atrial cardiomyocytes with Ca 2+ imaging, establishing a causal role for decreased SPEG in AF pathogenesis. Phosphoproteomics in hearts from SPEG cardiomyocyte knockout mice identified RyR2-S2367 as a novel kinase substrate of SPEG. Western blotting demonstrated that RyR2-S2367 phosphorylation was also decreased in patients with paroxysmal AF. RyR2-S2367A mice exhibited an increased susceptibility to pacing-induced AF, and aberrant atrial sarcoplasmic reticulum Ca 2+ leak, as well. In contrast, RyR2-S2367D mice were resistant to pacing-induced AF. Conclusions: Unlike other kinases (PKA, CaMKII) that increase RyR2 activity, SPEG phosphorylation reduces RyR2-mediated sarcoplasmic reticulum Ca 2+ release. Reduced SPEG levels and RyR2-S2367 phosphorylation typified patients with paroxysmal AF. Studies in S2367 knockin mouse models showed a causal relationship between reduced S2367 phosphorylation and AF susceptibility. Thus, modulating SPEG activity and phosphorylation levels of the novel S2367 site on RyR2 may represent a novel target for AF treatment.

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Hines, Kevin M., Vishalsingh Chaudhari, Kristen N. Edgeworth, Thomas G. Owens, and Maureen R. Hanson. "Absence of carbonic anhydrase in chloroplasts affects C3 plant development but not photosynthesis." Proceedings of the National Academy of Sciences 118, no. 33 (August 11, 2021): e2107425118. http://dx.doi.org/10.1073/pnas.2107425118.

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The enzyme carbonic anhydrase (CA), which catalyzes the interconversion of bicarbonate with carbon dioxide (CO2) and water, has been hypothesized to play a role in C3 photosynthesis. We identified two tobacco stromal CAs, β-CA1 and β-CA5, and produced CRISPR/Cas9 mutants affecting their encoding genes. While single knockout lines Δβ-ca1 and Δβ-ca5 had no striking phenotypic differences compared to wild type (WT) plants, Δβ-ca1ca5 leaves developed abnormally and exhibited large necrotic lesions even when supplied with sucrose. Leaf development of Δβ-ca1ca5 plants normalized at 9,000 ppm CO2. Leaves of Δβ-ca1ca5 mutants and WT that had matured in high CO2 had identical CO2 fixation rates and photosystem II efficiency. Fatty acids, which are formed through reactions with bicarbonate substrates, exhibited abnormal profiles in the chloroplast CA-less mutant. Emerging Δβ-ca1ca5 leaves produce reactive oxygen species in chloroplasts, perhaps due to lower nonphotochemical quenching efficiency compared to WT. Δβ-ca1ca5 seedling germination and development is negatively affected at ambient CO2. Transgenes expressing full-length β-CA1 and β-CA5 proteins complemented the Δβ-ca1ca5 mutation but inactivated (ΔZn-βCA1) and cytoplasm-localized (Δ62-βCA1) forms of β-CA1 did not reverse the growth phenotype. Nevertheless, expression of the inactivated ΔZn-βCA1 protein was able to restore the hypersensitive response to tobacco mosaic virus, while Δβ-ca1 and Δβ-ca1ca5 plants failed to show a hypersensitive response. We conclude that stromal CA plays a role in plant development, likely through providing bicarbonate for biosynthetic reactions, but stromal CA is not needed for maximal rates of photosynthesis in the C3 plant tobacco.

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Lawrence, C. Martin, Alexander Charbonneau, and Colin Gauvin. "Cyclic Tetra‐Adenylate (cA 4 ) Activates CRISPR Associated Transcription Factor Csa3, Providing Feedback Activation of Protospacer Acquisition and crRNA Expression." FASEB Journal 34, S1 (April 2020): 1. http://dx.doi.org/10.1096/fasebj.2020.34.s1.05969.

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Більше джерел

Дисертації з теми "CRISPR-Ca"

Demozzi, Michele. "Identification of novel active Cas9 orthologs from metagenomic data." Doctoral thesis, Università degli studi di Trento, 2022. http://hdl.handle.net/11572/337709.

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CRISPR-Cas is the state-of-the-art biological tool that allows precise and fast manipulation of the genetic information of cellular genomes. The translation of the CRISPR-Cas technology from in vitro studies into clinical applications highlighted a variety of limitations: the currently available systems are limited by their off-target activity, the availability of a Cas-specific PAM sequence next to the target and the size of the Cas protein. In particular, despite high levels of activity, the size of the CRISPR-SpCas9 editing machinery is not compatible with an all-in-one AAV delivery system and the genomic sequences that can be targeted are limited by the 3-NGG PAM-dependency of the SpCas9 protein. To further expand the CRISPR tools repertoire we turned to metagenomic data of the human microbiome to search for uncharacterized CRISPR-Cas9 systems and we identified a set of novel small Cas9 orthologs derived from the analysis of reconstructed bacterial metagenomes. In this thesis study, ten candidates were chosen according to their size (less than 1100aa). The PAM preference of all the ten orthologs was established exploiting a bacterial-based and an in vitro platform. We demonstrated that three of them are active nucleases in human cells and two out of the three showed robust editing levels at endogenous loci, outperforming SpCas9 at particular targets. We expect these new variants to be very useful in expanding the available genome editing tools both in vitro and in vivo. Knock-out-based Cas9 applications are very efficient but many times a precise control of the repair outcome through HDR-mediated gene targeting is required. To address this issue, we also developed an MS2-based reporter platform to measure the frequency of HDR events and evaluate novel HDR-modulating factors. The platform was validated and could allow the screening of libraries of proteins to assess their influence on the HDR pathway.

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Тези доповідей конференцій з теми "CRISPR-Ca"

Lee, Sanghoon, Changhong Yin, Janet Ayello, Carmella van de Ven, and Mitchell S. Cairo. "Abstract 3617: Clustered regularly interspaced short palindromic repeats (CRISPR)/CRISPR-associated (CAS) system mediated endogenous CD19 gene knockout model in burkitt lymphoma." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-3617.

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Winter, Jan, Marc Schwering, Benedikt Rauscher, Florian Heigwer, and Michael Boutros. "Abstract A10: CRISPR-AnalyzeR (caR): Web-based, interactive and exploratory analysis and documentation of pooled CRISPR/Cas9 screens." In Abstracts: AACR Precision Medicine Series: Opportunities and Challenges of Exploiting Synthetic Lethality in Cancer; January 4-7, 2017; San Diego, CA. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-8514.synthleth-a10.

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Ventura, Andrea. "Abstract IA25: Modeling cancer in the CRISPR era." In Abstracts: AACR Special Conference on the Evolving Landscape of Cancer Modeling; March 2-5, 2020; San Diego, CA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.camodels2020-ia25.

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Podolsky, M., C. Yang, C. Lizama-Valenzuela, M. McManus, and K. Atabai. "Genome-Wide CRISPR Screens Identify Novel Mediators of Cell-Mediated Collagen Degradation." In American Thoracic Society 2021 International Conference, May 14-19, 2021 - San Diego, CA. American Thoracic Society, 2021. http://dx.doi.org/10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a4357.

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Lu, Y., J. Lee, C. Moneypenny, N. Mohammad, A. Aranyos, and M. L. Brantly. "Enhanced mTOR Activity in CRISPR/Cas9 Gene-Edited PIZ Alpha-1 Antitrypsin Hepatocytes." In American Thoracic Society 2022 International Conference, May 13-18, 2022 - San Francisco, CA. American Thoracic Society, 2022. http://dx.doi.org/10.1164/ajrccm-conference.2022.205.1_meetingabstracts.a4665.

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Joung, J. Keith. "Abstract IA07: Defining, Optimizing, and Altering the Specificities of CRISPR-Cas Nucleases." In Abstracts: AACR Precision Medicine Series: Opportunities and Challenges of Exploiting Synthetic Lethality in Cancer; January 4-7, 2017; San Diego, CA. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-8514.synthleth-ia07.

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Staudt, Louis M. "Abstract IA09: Genome-wide CRISPR screens illuminate lymphoma pathogenesis and therapeutic resistance." In Abstracts: AACR Precision Medicine Series: Opportunities and Challenges of Exploiting Synthetic Lethality in Cancer; January 4-7, 2017; San Diego, CA. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-8514.synthleth-ia09.

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Zhou, Nanjiang, and Yin-Yuan Mo. "Abstract 461: Modulation of estrogen receptor (ER) and androgen receptor (AR) by a modified CRISPR-Cas9 system." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-461.

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Zhou, Wenrong, Min Long, Xi Li, Zhengang Peng, Qunsheng Ji, and Yong Cang. "Abstract A32: Screening for synthetic lethal interactions using customized epigenetic CRISPR-Cas9 libraries." In Abstracts: AACR Precision Medicine Series: Opportunities and Challenges of Exploiting Synthetic Lethality in Cancer; January 4-7, 2017; San Diego, CA. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-8514.synthleth-a32.

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Kimura, H., D. Francisco, M. Conway, A. Molzahn, N. Schaunaman, H. W. Chu, and M. Kraft. "CRISPR/Cas9-Mediated Gene Knockout Reveals the Mucin Regulating Function of CC16 in Human Distal Airway Epithelial Cells." In American Thoracic Society 2022 International Conference, May 13-18, 2022 - San Francisco, CA. American Thoracic Society, 2022. http://dx.doi.org/10.1164/ajrccm-conference.2022.205.1_meetingabstracts.a3260.

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