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Academic literature on the topic 'Pol01'

Author: Grafiati

Published: 29 July 2024

Last updated: 30 July 2024

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Journal articles on the topic "Pol01"

1

Perfecto-Avalos, Yocanxochitl, Jose R. Borbolla Escoboza, Luis M. Villela-Martiez, et al. "Correlation between FOXP3 Gene Polymorphisms in Donors, and the Severity of Acute Graft-Versus-Host Disease in Patients after Related Allogeneic Stem Cell Transplantation." Blood 110, no. 11 (2007): 3233. http://dx.doi.org/10.1182/blood.v110.11.3233.3233.

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Abstract INTRODUCTION: Acute Graft-versus-host disease (aGVHD) is a major complication of allogeneic stem cell transplantation (alloSCT). Risk factors include patient age, sex matching, CMV status and degree of match. Regulatory T cells are critical for immune tolerance processes such as aGVHD, and express the transcription factor FOXP3, a member of the forkhead/winged-helix family, identified as a key regulatory gene required for the development and activity of these cells. It has been suggested that genetic expression of FOXP3 is inversely correlated with the severity of the GVHD. We studied

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2

Pachlopnik Schmid, Jana, Roxane Lemoine, Nadine Nehme та ін. "Polymerase ε1 mutation in a human syndrome with facial dysmorphism, immunodeficiency, livedo, and short stature (“FILS syndrome”)". Journal of Experimental Medicine 209, № 13 (2012): 2323–30. http://dx.doi.org/10.1084/jem.20121303.

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DNA polymerase ε (Polε) is a large, four-subunit polymerase that is conserved throughout the eukaryotes. Its primary function is to synthesize DNA at the leading strand during replication. It is also involved in a wide variety of fundamental cellular processes, including cell cycle progression and DNA repair/recombination. Here, we report that a homozygous single base pair substitution in POLE1 (polymerase ε 1), encoding the catalytic subunit of Polε, caused facial dysmorphism, immunodeficiency, livedo, and short stature (“FILS syndrome”) in a large, consanguineous family. The mutation resulte

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3

TUBAU, SUSAGNA. "The asymmetric behavior of English negative quantifiers in negative sentences." Journal of Linguistics 56, no. 4 (2020): 775–806. http://dx.doi.org/10.1017/s0022226719000495.

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In this paper, the unexpected behavior of object negative quantifiers in some diagnostic tests of sentential negation is accounted for within a Minimalist framework assuming that: (i) negative quantifiers decompose into negation and an existential quantifier; (ii) negative quantifiers are multidominant phrase markers, as Parallel Merge allows the verb to c-select their existential part but not their negative part, thus giving negation remerge flexibility; (iii) tag questions involve or-coordination of TPs, and neither/so clauses involve and-coordination of TPs; (iv) two positions for sententia

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4

Shimada, Kenji, Monika Tsai-Pflugfelder, Niloofar Davoodi Vijeh Motlagh, et al. "The stabilized Pol31–Pol3 interface counteracts Pol32 ablation with differential effects on repair." Life Science Alliance 4, no. 9 (2021): e202101138. http://dx.doi.org/10.26508/lsa.202101138.

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DNA polymerase δ, which contains the catalytic subunit, Pol3, Pol31, and Pol32, contributes both to DNA replication and repair. The deletion of pol31 is lethal, and compromising the Pol3–Pol31 interaction domains confers hypersensitivity to cold, hydroxyurea (HU), and methyl methanesulfonate, phenocopying pol32Δ. We have identified alanine-substitutions in pol31 that suppress these deficiencies in pol32Δ cells. We characterize two mutants, pol31-T415A and pol31-W417A, which map to a solvent-exposed loop that mediates Pol31–Pol3 and Pol31–Rev3 interactions. The pol31-T415A substitution compromi

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5

Miyabayashi, Hiroka, Hiroyuki D. Sakai, and Norio Kurosawa. "DNA Polymerase B1 Binding Protein 1 Is Important for DNA Repair by Holoenzyme PolB1 in the Extremely Thermophilic Crenarchaeon Sulfolobus acidocaldarius." Microorganisms 9, no. 2 (2021): 439. http://dx.doi.org/10.3390/microorganisms9020439.

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DNA polymerase B1 (PolB1) is a member of the B-family DNA polymerase family and is a replicative DNA polymerase in Crenarchaea. PolB1 is responsible for the DNA replication of both the leading and lagging strands in the thermophilic crenarchaeon Sulfolobus acidocaldarius. Recently, two subunits, PolB1-binding protein (PBP)1 and PBP2, were identified in Saccharolobus solfataricus. Previous in vitro studies suggested that PBP1 and PBP2 influence the core activity of apoenzyme PolB1 (apo-PolB1). PBP1 contains a C-terminal acidic tail and modulates the strand-displacement synthesis activity of Pol

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6

Yao, Jianfei, Shiying Dang, Lifeng Li, et al. "Characteristics of POLE and POLD1 gene variations in Chinese cancer patients." Journal of Clinical Oncology 37, no. 15_suppl (2019): e14031-e14031. http://dx.doi.org/10.1200/jco.2019.37.15_suppl.e14031.

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e14031 Background: POLE and POLD1 gene variations have been suggested as potential markers for immunotherapy due to their significant association with the tumor mutation burden (TMB), an effective indicator for response prediction in immunotherapy. Methods: In this study, we systematically studied the spectrum and characteristics of POLE and POLD1 gene variations from 1,392 Chinese cancer patients, and their correlation with existing immunotherapeutic markers and cancer associated genes. Results: We found that the frequency of POLE variations was not statistically different from that in COSMIC

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7

Tian, Junjie, Cheng Cheng, Jianguo Gao, et al. "POLD1 as a Prognostic Biomarker Correlated with Cell Proliferation and Immune Infiltration in Clear Cell Renal Cell Carcinoma." International Journal of Molecular Sciences 24, no. 7 (2023): 6849. http://dx.doi.org/10.3390/ijms24076849.

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DNA polymerase delta 1 catalytic subunit (POLD1) plays a vital role in genomic copy with high fidelity and DNA damage repair processes. However, the prognostic value of POLD1 and its relationship with tumor immunity in clear cell renal cell carcinoma (ccRCC) remains to be further explored. Transcriptional data sets and clinical information were obtained from the TCGA, ICGC, and GEO databases. Differentially expressed genes (DEGs) were derived from the comparison between the low and high POLD1 expression groups in the TCGA–KIRC cohort. KEGG and gene ontology (GO) analyses were performed for tho

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8

Coston, Tucker, Elizabeth Mauer, Jeremy Clifton Jones, et al. "Characterizing the genomic landscape of POLE/POLD1-mutated colorectal adenocarcinoma." Journal of Clinical Oncology 41, no. 4_suppl (2023): 199. http://dx.doi.org/10.1200/jco.2023.41.4_suppl.199.

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199 Background: The progression of neoplasia in colorectal cancer (CRC) has been well characterized, with the evolution typically involving mutations in APC, KRAS, and p53, among others. POLE/POLD1 genes encode for proteins essential in enzymatic DNA polymerase function, yet POLE/POLD1 mutations in tumors are poorly characterized. Pathogenic mutations in POLE/POLD1 lead to decreased fidelity of DNA replication, resulting in a high tumor mutational burden (TMB-H) independent of deficient mismatch repair (dMMR) and high microsatellite instability (MSI-H). Studies have shown associations between

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9

Jia, Yongning, Yaqun Xin, Hongling Yuan, et al. "Abstract 5751: Comprehensive analysis of POLE/POLD1 variants, MMR deficient/MSI, and tumor mutational burden in Chinese population." Cancer Research 82, no. 12_Supplement (2022): 5751. http://dx.doi.org/10.1158/1538-7445.am2022-5751.

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Abstract Background: Mutations in genes encoding DNA polymerase epsilon (POLE) and delta 1 (POLD1) can lead to defects in the DNA replication, resulting in a hypermutated tumor phenotype, which might help identify potential responders to immunotherapy. This study aims to comprehensively investigate the different variants of POLE/POLD1 mutants and how it related to MSI/MMR status and TMB levels within a large Chinese population. Methods:Among 15640 Chinese patients who underwent NGS testing, the prevalence of POLE/POLD1 mutants was analyzed and the high frequencies of POLE/POLD1 variants as wel

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10

Syed, Masood Pasha, Morgan Ferrell, Svea Cheng, et al. "Molecular and clinical characteristics of POLE/POLD1 alterations among patients with colorectal cancer." Journal of Clinical Oncology 42, no. 3_suppl (2024): 184. http://dx.doi.org/10.1200/jco.2024.42.3_suppl.184.

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184 Background: POLE and POLD1 alterations (DNA polymerase ε and DNA polymerase δ) are key biomarkers of immune response for patients with MSS colorectal cancers (CRC). The clinical and molecular characteristics of POLE/POLD1 alterations are not yet well defined across CRCs. In this study, we investigated the clinical/molecular features of POLE and POLD1 alterations and its association with MSI-H CRC. Methods: All the patients and mutation data were selected from the cBioPortal database (https://www.cbioportal.org). All nonsynonymous mutations including missense, frameshift, nonsense, nonstop,

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