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Showing 9985 to 9996 of 11435 entries
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Capsid-CPSF6 interaction: Master regulator of nuclear HIV-1 positioning and integration.

Journal of life sciences (Westlake Village, Calif.)

Achuthan V, Perreira JM, Ahn JJ, Brass AL, Engelman AN.
PMID: 31448372
J Life Sci (Westlake Village). 2019 Jun;1(1):39-45. doi: 10.36069/jols/20190604.

HIV-1 integration favors active chromatin, which is primarily mediated through interactions between the viral capsid and integrase proteins with host factors cleavage and polyadenylation specificity factor 6 (CPSF6) and lens epithelium-derived growth factor/p75, respectively. Previously published image-based studies had...

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Achuthan V, Perreira JM, Ahn JJ, et al. Capsid-CPSF6 interaction: Master regulator of nuclear HIV-1 positioning and integration. J Life Sci (Westlake Village). 2019;1(1):39-45doi: 10.36069/jols/20190604.
Achuthan, V., Perreira, J. M., Ahn, J. J., Brass, A. L., & Engelman, A. N. (2019). Capsid-CPSF6 interaction: Master regulator of nuclear HIV-1 positioning and integration. Journal of life sciences (Westlake Village, Calif.), 1(1), 39-45. https://doi.org/10.36069/jols/20190604
Achuthan, Vasudevan, et al. "Capsid-CPSF6 interaction: Master regulator of nuclear HIV-1 positioning and integration." Journal of life sciences (Westlake Village, Calif.) vol. 1,1 (2019): 39-45. doi: https://doi.org/10.36069/jols/20190604
Achuthan V, Perreira JM, Ahn JJ, Brass AL, Engelman AN. Capsid-CPSF6 interaction: Master regulator of nuclear HIV-1 positioning and integration. J Life Sci (Westlake Village). 2019 Jun;1(1):39-45. doi: 10.36069/jols/20190604. PMID: 31448372; PMCID: PMC6707730.
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Ultrastructure of the gametolytic gland and seminal receptacle in Hypselodoris messinensis (Gastropoda, Opisthobranchia).

Journal of morphology

Medina A, Griffond B, Garcia-Gomez JC, Garcia FJ.
PMID: 29898573
J Morphol. 1988 Jan;195(1):95-102. doi: 10.1002/jmor.1051950109.

The gametolytic gland of Hypselodoris messinensis is a voluminous globular structure that encloses a large mass of degenerative gametes, especially waste exogenous sperm. The epithelial cells of this organ show some features characteristic of secretory cells and probably release...

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Medina A, Griffond B, Garcia-Gomez JC, et al. Ultrastructure of the gametolytic gland and seminal receptacle in Hypselodoris messinensis (Gastropoda, Opisthobranchia). J Morphol. 1988;195(1):95-102doi: 10.1002/jmor.1051950109.
Medina, A., Griffond, B., Garcia-Gomez, J. C., & Garcia, F. J. (1988). Ultrastructure of the gametolytic gland and seminal receptacle in Hypselodoris messinensis (Gastropoda, Opisthobranchia). Journal of morphology, 195(1), 95-102. https://doi.org/10.1002/jmor.1051950109
Medina, A, et al. "Ultrastructure of the gametolytic gland and seminal receptacle in Hypselodoris messinensis (Gastropoda, Opisthobranchia)." Journal of morphology vol. 195,1 (1988): 95-102. doi: https://doi.org/10.1002/jmor.1051950109
Medina A, Griffond B, Garcia-Gomez JC, Garcia FJ. Ultrastructure of the gametolytic gland and seminal receptacle in Hypselodoris messinensis (Gastropoda, Opisthobranchia). J Morphol. 1988 Jan;195(1):95-102. doi: 10.1002/jmor.1051950109. PMID: 29898573.
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Cancer Stem Cell-Inducing Media Activates Senescence Reprogramming in Fibroblasts.

Cancers

Perrigue PM, Rakoczy M, Pawlicka KP, Belter A, Giel-Pietraszuk M, Naskręt-Barciszewska M, Barciszewski J, Figlerowicz M.
PMID: 32629974
Cancers (Basel). 2020 Jun 30;12(7). doi: 10.3390/cancers12071745.

Cellular senescence is a tumor-suppressive mechanism blocking cell proliferation in response to stress. However, recent evidence suggests that senescent tumor cells can re-enter the cell cycle to become cancer stem cells, leading to relapse after cancer chemotherapy treatment. Understanding...

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Perrigue PM, Rakoczy M, Pawlicka KP, et al. Cancer Stem Cell-Inducing Media Activates Senescence Reprogramming in Fibroblasts. Cancers (Basel). 2020;12(7)doi: 10.3390/cancers12071745.
Perrigue, P. M., Rakoczy, M., Pawlicka, K. P., Belter, A., Giel-Pietraszuk, M., Naskręt-Barciszewska, M., Barciszewski, J., & Figlerowicz, M. (2020). Cancer Stem Cell-Inducing Media Activates Senescence Reprogramming in Fibroblasts. Cancers, 12(7), . https://doi.org/10.3390/cancers12071745
Perrigue, Patrick M, et al. "Cancer Stem Cell-Inducing Media Activates Senescence Reprogramming in Fibroblasts." Cancers vol. 12,7 (2020). doi: https://doi.org/10.3390/cancers12071745
Perrigue PM, Rakoczy M, Pawlicka KP, Belter A, Giel-Pietraszuk M, Naskręt-Barciszewska M, Barciszewski J, Figlerowicz M. Cancer Stem Cell-Inducing Media Activates Senescence Reprogramming in Fibroblasts. Cancers (Basel). 2020 Jun 30;12(7). doi: 10.3390/cancers12071745. PMID: 32629974; PMCID: PMC7409320.
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PARP1 Co-Regulates EP300-BRG1-Dependent Transcription of Genes Involved in Breast Cancer Cell Proliferation and DNA Repair.

Cancers

Sobczak M, Pitt AR, Spickett CM, Robaszkiewicz A.
PMID: 31614656
Cancers (Basel). 2019 Oct 11;11(10). doi: 10.3390/cancers11101539.

BRG1, an active subunit of the SWI/SNF chromatin-remodeling complex, enables the EP300-dependent transcription of proliferation and DNA repair genes from their E2F/CpG-driven promoters in breast cancer cells. In the current study, we show that BRG1-EP300 complexes are accompanied by...

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Sobczak M, Pitt AR, Spickett CM, et al. PARP1 Co-Regulates EP300-BRG1-Dependent Transcription of Genes Involved in Breast Cancer Cell Proliferation and DNA Repair. Cancers (Basel). 2019;11(10)doi: 10.3390/cancers11101539.
Sobczak, M., Pitt, A. R., Spickett, C. M., & Robaszkiewicz, A. (2019). PARP1 Co-Regulates EP300-BRG1-Dependent Transcription of Genes Involved in Breast Cancer Cell Proliferation and DNA Repair. Cancers, 11(10), . https://doi.org/10.3390/cancers11101539
Sobczak, Maciej, et al. "PARP1 Co-Regulates EP300-BRG1-Dependent Transcription of Genes Involved in Breast Cancer Cell Proliferation and DNA Repair." Cancers vol. 11,10 (2019). doi: https://doi.org/10.3390/cancers11101539
Sobczak M, Pitt AR, Spickett CM, Robaszkiewicz A. PARP1 Co-Regulates EP300-BRG1-Dependent Transcription of Genes Involved in Breast Cancer Cell Proliferation and DNA Repair. Cancers (Basel). 2019 Oct 11;11(10). doi: 10.3390/cancers11101539. PMID: 31614656; PMCID: PMC6826995.
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Interaction of RSC Chromatin Remodeling Complex with Nucleosomes Is Modulated by H3 K14 Acetylation and H2B SUMOylation In Vivo.

iScience

Jain N, Tamborrini D, Evans B, Chaudhry S, Wilkins BJ, Neumann H.
PMID: 32623337
iScience. 2020 Jul 24;23(7):101292. doi: 10.1016/j.isci.2020.101292. Epub 2020 Jun 20.

Chromatin remodeling complexes are multi-subunit nucleosome translocases that reorganize chromatin in the context of DNA replication, repair, and transcription. To understand how these complexes find their target sites on chromatin, we use genetically encoded photo-cross-linker amino acids to map...

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Jain N, Tamborrini D, Evans B, et al. Interaction of RSC Chromatin Remodeling Complex with Nucleosomes Is Modulated by H3 K14 Acetylation and H2B SUMOylation In Vivo. iScience. 2020;23(7):101292doi: 10.1016/j.isci.2020.101292.
Jain, N., Tamborrini, D., Evans, B., Chaudhry, S., Wilkins, B. J., & Neumann, H. (2020). Interaction of RSC Chromatin Remodeling Complex with Nucleosomes Is Modulated by H3 K14 Acetylation and H2B SUMOylation In Vivo. iScience, 23(7), 101292. https://doi.org/10.1016/j.isci.2020.101292
Jain, Neha, et al. "Interaction of RSC Chromatin Remodeling Complex with Nucleosomes Is Modulated by H3 K14 Acetylation and H2B SUMOylation In Vivo." iScience vol. 23,7 (2020): 101292. doi: https://doi.org/10.1016/j.isci.2020.101292
Jain N, Tamborrini D, Evans B, Chaudhry S, Wilkins BJ, Neumann H. Interaction of RSC Chromatin Remodeling Complex with Nucleosomes Is Modulated by H3 K14 Acetylation and H2B SUMOylation In Vivo. iScience. 2020 Jul 24;23(7):101292. doi: 10.1016/j.isci.2020.101292. Epub 2020 Jun 20. PMID: 32623337; PMCID: PMC7334588.
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Histone H3 Mutations: An Updated View of Their Role in Chromatin Deregulation and Cancer.

Cancers

Lowe BR, Maxham LA, Hamey JJ, Wilkins MR, Partridge JF.
PMID: 31086012
Cancers (Basel). 2019 May 13;11(5). doi: 10.3390/cancers11050660.

In this review, we describe the attributes of histone H3 mutants identified in cancer. H3 mutants were first identified in genes encoding H3.3, in pediatric high-grade glioma, and subsequently in chondrosarcomas and giant cell tumors of bone (GCTB) in...

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Lowe BR, Maxham LA, Hamey JJ, et al. Histone H3 Mutations: An Updated View of Their Role in Chromatin Deregulation and Cancer. Cancers (Basel). 2019;11(5)doi: 10.3390/cancers11050660.
Lowe, B. R., Maxham, L. A., Hamey, J. J., Wilkins, M. R., & Partridge, J. F. (2019). Histone H3 Mutations: An Updated View of Their Role in Chromatin Deregulation and Cancer. Cancers, 11(5), . https://doi.org/10.3390/cancers11050660
Lowe, Brandon R, et al. "Histone H3 Mutations: An Updated View of Their Role in Chromatin Deregulation and Cancer." Cancers vol. 11,5 (2019). doi: https://doi.org/10.3390/cancers11050660
Lowe BR, Maxham LA, Hamey JJ, Wilkins MR, Partridge JF. Histone H3 Mutations: An Updated View of Their Role in Chromatin Deregulation and Cancer. Cancers (Basel). 2019 May 13;11(5). doi: 10.3390/cancers11050660. PMID: 31086012; PMCID: PMC6562757.
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FGFR2-mediated phosphorylation of PTEN at tyrosine 240 contributes to the radioresistance of glioma.

Journal of cell communication and signaling

Yan Y, Li Z, Zeng S, Wang X, Gong Z, Xu Z.
PMID: 31025173
J Cell Commun Signal. 2019 Sep;13(3):279-280. doi: 10.1007/s12079-019-00518-6. Epub 2019 Apr 25.

Ionizing radiation (IR) is a standard-of-care treatment for glioma patients; however, the clinical efficacy is limited due to therapeutic resistance. A recent study published by Ma et al. (Cancer Cell 35:504-518, 2019) reported that the phosphorylation of phosphatase and...

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Yan Y, Li Z, Zeng S, et al. FGFR2-mediated phosphorylation of PTEN at tyrosine 240 contributes to the radioresistance of glioma. J Cell Commun Signal. 2019;13(3):279-280doi: 10.1007/s12079-019-00518-6.
Yan, Y., Li, Z., Zeng, S., Wang, X., Gong, Z., & Xu, Z. (2019). FGFR2-mediated phosphorylation of PTEN at tyrosine 240 contributes to the radioresistance of glioma. Journal of cell communication and signaling, 13(3), 279-280. https://doi.org/10.1007/s12079-019-00518-6
Yan, Yuanliang, et al. "FGFR2-mediated phosphorylation of PTEN at tyrosine 240 contributes to the radioresistance of glioma." Journal of cell communication and signaling vol. 13,3 (2019): 279-280. doi: https://doi.org/10.1007/s12079-019-00518-6
Yan Y, Li Z, Zeng S, Wang X, Gong Z, Xu Z. FGFR2-mediated phosphorylation of PTEN at tyrosine 240 contributes to the radioresistance of glioma. J Cell Commun Signal. 2019 Sep;13(3):279-280. doi: 10.1007/s12079-019-00518-6. Epub 2019 Apr 25. PMID: 31025173; PMCID: PMC6732132.
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Melatonin ameliorates testicular damages induced by nicotine in mice.

Iranian journal of basic medical sciences

Mohammadghasemi F, Jahromi SK.
PMID: 29942456
Iran J Basic Med Sci. 2018 Jun;21(6):639-644. doi: 10.22038/IJBMS.2018.28111.6829.

OBJECTIVES: Nicotine as a toxic substance leads to impairment of the reproductive system function. The aim of this study was to evaluate effects of melatonin on testicular alterations, sperm nuclear integrity, and epididymal sperm parameters in mice treated with...

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Mohammadghasemi F, Jahromi SK. Melatonin ameliorates testicular damages induced by nicotine in mice. Iran J Basic Med Sci. 2018;21(6):639-644doi: 10.22038/IJBMS.2018.28111.6829.
Mohammadghasemi, F., & Jahromi, S. K. (2018). Melatonin ameliorates testicular damages induced by nicotine in mice. Iranian journal of basic medical sciences, 21(6), 639-644. https://doi.org/10.22038/IJBMS.2018.28111.6829
Mohammadghasemi, Fahimeh, and Jahromi, Sina Khajeh. "Melatonin ameliorates testicular damages induced by nicotine in mice." Iranian journal of basic medical sciences vol. 21,6 (2018): 639-644. doi: https://doi.org/10.22038/IJBMS.2018.28111.6829
Mohammadghasemi F, Jahromi SK. Melatonin ameliorates testicular damages induced by nicotine in mice. Iran J Basic Med Sci. 2018 Jun;21(6):639-644. doi: 10.22038/IJBMS.2018.28111.6829. PMID: 29942456; PMCID: PMC6015250.
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Dendritic Cells Actively Limit Interleukin-10 Production Under Inflammatory Conditions .

Frontiers in immunology

Søndergaard JN, van Heeringen SJ, Looman MWG, Tang C, Triantis V, Louche P, Janssen-Megens EM, Sieuwerts AM, Martens JWM, Logie C, Stunnenberg HG, Ansems M, Adema GJ.
PMID: 29988341
Front Immunol. 2018 Jun 22;9:1420. doi: 10.3389/fimmu.2018.01420. eCollection 2018.

Dendritic cell (DC)-based immunotherapy makes use of the DC's ability to direct the adaptive immune response toward activation or inhibition. DCs perform this immune orchestration in part by secretion of selected cytokines. The most potent anti-inflammatory cytokine interleukin-10 (IL-10)...

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Søndergaard JN, van Heeringen SJ, Looman MWG, et al. Dendritic Cells Actively Limit Interleukin-10 Production Under Inflammatory Conditions . Front Immunol. 2018;9:1420doi: 10.3389/fimmu.2018.01420.
Søndergaard, J. N., van Heeringen, S. J., Looman, M. W. G., Tang, C., Triantis, V., Louche, P., Janssen-Megens, E. M., Sieuwerts, A. M., Martens, J. W. M., Logie, C., Stunnenberg, H. G., Ansems, M., & Adema, G. J. (2018). Dendritic Cells Actively Limit Interleukin-10 Production Under Inflammatory Conditions . Frontiers in immunology, 91420. https://doi.org/10.3389/fimmu.2018.01420
Søndergaard, Jonas Nørskov, et al. "Dendritic Cells Actively Limit Interleukin-10 Production Under Inflammatory Conditions ." Frontiers in immunology vol. 9 (2018): 1420. doi: https://doi.org/10.3389/fimmu.2018.01420
Søndergaard JN, van Heeringen SJ, Looman MWG, Tang C, Triantis V, Louche P, Janssen-Megens EM, Sieuwerts AM, Martens JWM, Logie C, Stunnenberg HG, Ansems M, Adema GJ. Dendritic Cells Actively Limit Interleukin-10 Production Under Inflammatory Conditions . Front Immunol. 2018 Jun 22;9:1420. doi: 10.3389/fimmu.2018.01420. eCollection 2018. PMID: 29988341; PMCID: PMC6023963.
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Nucleosome Remodeling by Fun30.

Frontiers in molecular biosciences

Bantele SCS, Pfander B.
PMID: 31555662
Front Mol Biosci. 2019 Sep 04;6:78. doi: 10.3389/fmolb.2019.00078. eCollection 2019.

Many cellular pathways are dedicated to maintain the integrity of the genome. In eukaryotes, the underlying DNA transactions occur in the context of chromatin. Cells utilize chromatin and its dynamic nature to regulate those genome integrity pathways. Accordingly, chromatin...

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Bantele SCS, Pfander B. Nucleosome Remodeling by Fun30. Front Mol Biosci. 2019;6:78doi: 10.3389/fmolb.2019.00078.
Bantele, S. C. S., & Pfander, B. (2019). Nucleosome Remodeling by Fun30. Frontiers in molecular biosciences, 678. https://doi.org/10.3389/fmolb.2019.00078
Bantele, Susanne C S, and Pfander, Boris. "Nucleosome Remodeling by Fun30." Frontiers in molecular biosciences vol. 6 (2019): 78. doi: https://doi.org/10.3389/fmolb.2019.00078
Bantele SCS, Pfander B. Nucleosome Remodeling by Fun30. Front Mol Biosci. 2019 Sep 04;6:78. doi: 10.3389/fmolb.2019.00078. eCollection 2019. PMID: 31555662; PMCID: PMC6737033.
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Towards a Better Understanding of Cohesin Mutations in AML.

Frontiers in oncology

Cuartero S, Innes AJ, Merkenschlager M.
PMID: 31552185
Front Oncol. 2019 Sep 09;9:867. doi: 10.3389/fonc.2019.00867. eCollection 2019.

Classical driver mutations in acute myeloid leukemia (AML) typically affect regulators of cell proliferation, differentiation, and survival. The selective advantage of increased proliferation, improved survival, and reduced differentiation on leukemia progression is immediately obvious. Recent large-scale sequencing efforts have...

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Cuartero S, Innes AJ, Merkenschlager M. Towards a Better Understanding of Cohesin Mutations in AML. Front Oncol. 2019;9:867doi: 10.3389/fonc.2019.00867.
Cuartero, S., Innes, A. J., & Merkenschlager, M. (2019). Towards a Better Understanding of Cohesin Mutations in AML. Frontiers in oncology, 9867. https://doi.org/10.3389/fonc.2019.00867
Cuartero, Sergi, et al. "Towards a Better Understanding of Cohesin Mutations in AML." Frontiers in oncology vol. 9 (2019): 867. doi: https://doi.org/10.3389/fonc.2019.00867
Cuartero S, Innes AJ, Merkenschlager M. Towards a Better Understanding of Cohesin Mutations in AML. Front Oncol. 2019 Sep 09;9:867. doi: 10.3389/fonc.2019.00867. eCollection 2019. PMID: 31552185; PMCID: PMC6746210.
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Global profiling of O-GlcNAcylated and/or phosphorylated proteins in hepatoblastoma.

Signal transduction and targeted therapy

Song H, Ma J, Bian Z, Chen S, Zhu J, Wang J, Huang N, Yin M, Sun F, Xu M, Pan Q.
PMID: 31637018
Signal Transduct Target Ther. 2019 Oct 11;4:40. doi: 10.1038/s41392-019-0067-4. eCollection 2019.

O-linked-β-N-acetylglucosamine (O-GlcNAc) glycosylation (O-GlcNAcylation) and phosphorylation are critical posttranslational modifications that are involved in regulating the functions of proteins involved in tumorigenesis and the development of various solid tumors. However, a detailed characterization of the patterns of these modifications...

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Song H, Ma J, Bian Z, et al. Global profiling of O-GlcNAcylated and/or phosphorylated proteins in hepatoblastoma. Signal Transduct Target Ther. 2019;4:40doi: 10.1038/s41392-019-0067-4.
Song, H., Ma, J., Bian, Z., Chen, S., Zhu, J., Wang, J., Huang, N., Yin, M., Sun, F., Xu, M., & Pan, Q. (2019). Global profiling of O-GlcNAcylated and/or phosphorylated proteins in hepatoblastoma. Signal transduction and targeted therapy, 440. https://doi.org/10.1038/s41392-019-0067-4
Song, Hang, et al. "Global profiling of O-GlcNAcylated and/or phosphorylated proteins in hepatoblastoma." Signal transduction and targeted therapy vol. 4 (2019): 40. doi: https://doi.org/10.1038/s41392-019-0067-4
Song H, Ma J, Bian Z, Chen S, Zhu J, Wang J, Huang N, Yin M, Sun F, Xu M, Pan Q. Global profiling of O-GlcNAcylated and/or phosphorylated proteins in hepatoblastoma. Signal Transduct Target Ther. 2019 Oct 11;4:40. doi: 10.1038/s41392-019-0067-4. eCollection 2019. PMID: 31637018; PMCID: PMC6799812.
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Showing 9985 to 9996 of 11435 entries