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Relevant bibliographies by topics / TET protease

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Journal articles

Academic literature on the topic 'TET protease'

Author: Grafiati

Published: 4 May 2024

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Journal articles on the topic "TET protease"

1

Ishikawa, Chika, Tatsuya Tsuda, Hiroe Konishi, Noboru Nakagawa, and Kiyofumi Yamanishi. "Tetracyclines Modulate Protease-Activated Receptor 2-Mediated Proinflammatory Reactions in Epidermal Keratinocytes." Antimicrobial Agents and Chemotherapy 53, no. 5 (2009): 1760–65. http://dx.doi.org/10.1128/aac.01540-08.

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ABSTRACT In addition to their antibiotic effects, tetracyclines have anti-inflammatory action that is often beneficial in the control of inflammatory skin disorders. In this study, we examined the effects of tetracycline (TET) and two of its derivatives, doxycycline (DOX) and minocycline (MIN), on the production of interleukin-8 (IL-8) elicited by the activation of protease-activated receptor 2 (PAR2) in normal human epidermal keratinocytes (NHEK). In NHEK, the production of IL-8 stimulated by an agonist peptide of PAR2, SLIGKIV-NH2, at 100 μM was significantly reduced by TET, DOX, or MIN at 5

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2

Wang, Chun-hui, Jia-min Yang, Yu-bo Guo, Jing Shen, and Xiao-hua Pei. "Anticancer Activity of Tetrandrine by Inducing Apoptosis in Human Breast Cancer Cell Line MDA-MB-231 In Vivo." Evidence-Based Complementary and Alternative Medicine 2020 (June 30, 2020): 1–11. http://dx.doi.org/10.1155/2020/6823520.

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Tetrandrine (TET) is an alkaloid extracted from a traditional Chinese medicinal plant. It exerts remarkable anticancer activity and induces apoptotic cell death in various human cancer cells. The present study aimed to investigate the effects of TET on the inhibition of tumor growth and the induction of apoptosis in MDA-MB-231 breast cancer in xenograft mice. Tumor weight and volume were measured. The histopathological changes in the tumor tissue were observed. Immunohistochemistry analysis of Bcl-2-associated X protein (Bax) and B-cell lymphoma/leukemia-2 (Bcl-2) was carried out. The expressi

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3

Borissenko, Ljudmila, and Michael Groll. "Crystal Structure of TET Protease Reveals Complementary Protein Degradation Pathways in Prokaryotes." Journal of Molecular Biology 346, no. 5 (2005): 1207–19. http://dx.doi.org/10.1016/j.jmb.2004.12.056.

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4

Chow, W. A., S. Guo, and F. Valdes-Albini. "HIV protease inhibitor (PI) therapy for liposarcoma." Journal of Clinical Oncology 24, no. 18_suppl (2006): 9564. http://dx.doi.org/10.1200/jco.2006.24.18_suppl.9564.

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9564 Background: Liposarcomas are the second most common soft-tissue sarcoma. Highly-active anti-retroviral therapy (HAART) with HIV PIs results in “HIV-1 protease inhibitor associated lipodystrophy syndrome,” characterized by peripheral fat wasting, central fat accumulation, insulin resistance, and hyperlipidemia. Based upon this syndrome, we hypothesized that HIV PIs might represent a novel liposarcoma therapy. Methods: SW872, LiSa-2, and FU-DDLS-1 liposarcoma, and control 293 embryonic kidney and HT1080 fibrosarcoma cell lines were treated with HIV PIs and subjected to cellular and molecula

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5

Chen, S., D. O. Henry, and M. K. Wong. "The biologic therapy of prostate cancer using plasminogen activator inhibitor-1 (PAI-1)." Journal of Clinical Oncology 24, no. 18_suppl (2006): 14596. http://dx.doi.org/10.1200/jco.2006.24.18_suppl.14596.

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14596 Background: Treating prostate cancer through the expression of intrinsic biologic modifiers is a relatively unexplored aspect of prostate cancer therapy. Plasminogen Activator Inhibitor-1 (PAI-1) is expressed at low levels in prostate cancer cells. PAI-1 is both an anti-angiogenesis agent, and also potently inhibits tumor proteases responsible for tumor invasion and metastases such as uPA and tPA. Thus we hypothesized that stimulation of tumor endogenous PAI-1 would result in a particularly powerful and profound prostate cancer regression. We present proof-of-concept from our experimenta

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6

Borissenko, Ljudmila, and Michael Groll. "Corrigendum to “Crystal Structure of TET Protease Reveals Complementary Protein Degradation Pathways in Prokaryotes” [J. Mol. Biol. (2005) 346, 1207–1219]." Journal of Molecular Biology 351, no. 1 (2005): 247. http://dx.doi.org/10.1016/j.jmb.2005.03.032.

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7

Byarugaba, Denis K., Godfrey Wokorach, Stephen Alafi, et al. "Whole Genome Sequencing Reveals High Genetic Diversity, Diverse Repertoire of Virulence-Associated Genes and Limited Antibiotic Resistance Genes among Commensal Escherichia coli from Food Animals in Uganda." Microorganisms 11, no. 8 (2023): 1868. http://dx.doi.org/10.3390/microorganisms11081868.

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Commensal Escherichia coli with broad repertoire of virulence and antimicrobial resistance (AMR) genes pose serious public health risks as reservoirs of AMR and virulence. This study undertook whole genome characterization of commensal E. coli from food-producing animals in Uganda to investigate their genome variability (resistome and virulome). We established that the E. coli had high genomic diversity with 38 sequence types, 24 FimH types, and 33 O-antigen serotypes randomly distributed within three phylogroups (A, B1, and E). A greater proportion (≥93.65%) of the E. coli were resistant to a

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8

Maghsoudi, Nader, Narges Kh Tafreshi, Fariba Khodagholi, et al. "Targeting enteroviral 2A protease by a 16-mer synthetic peptide: Inhibition of 2Apro-induced apoptosis in a stable Tet-on HeLa cell line." Virology 399, no. 1 (2010): 39–45. http://dx.doi.org/10.1016/j.virol.2009.12.017.

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9

Aprikyan, Andrew A. G., Tomas Vaisar, Vahagn Makaryan, and Jay Heinecke. "Cellular Model of Severe Congenital Neutropenia Reveals the Molecular Mechanism of Mutant Elastase-Mediated Agranulocytosis." Blood 104, no. 11 (2004): 1453. http://dx.doi.org/10.1182/blood.v104.11.1453.1453.

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Abstract Severe congenital neutropenia (SCN) or Kostmann’s syndrome defines an inheritable hematopoietic disorder of an impaired neutrophil production in the bone marrow due to a “maturation arrest” at promyelocytic stage of differentiation in the marrow. SCN patients have recurring severe infections and may evolve to develop leukemia. We reported accelerated apoptosis and cell cycle arrest of bone marrow-derived myeloid progenitor cells in SCN patients with acquired, autosomal dominant, as well as autosomal recessive inheritance. We also reported that approximately 80% of these patients have

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10

Aprikyan, Andrew A., Tomas Vaisar, Vahagn Makaryan, and Jay Heinecke. "A Model of Severe Congenital Neutropenia Reveals Signaling Pathways Mediating Mutant Elastase-Triggered Agranulocytosis." Blood 106, no. 11 (2005): 3070. http://dx.doi.org/10.1182/blood.v106.11.3070.3070.

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Abstract Severe congenital neutropenia (SCN; Kostmann’s syndrome or infantile genetic agranulocytosis) defines an inheritable hematopoietic disorder of impaired neutrophil production due to a “maturation arrest” at the promyelocytic stage of differentiation in the bone marrow. SCN patients have recurring severe infections and often develop acute myelogenous leukemia. We and others reported accelerated apoptosis and cell cycle arrest of bone marrow-derived myeloid progenitor cells in SCN patients with autosomal dominant and autosomal recessive inheritance. Heterozygous mutations in the neutroph

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