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  1. Article ; Online: NF-κB signaling in neoplastic transition from epithelial to mesenchymal phenotype.

    Oh, Amy / Pardo, Makayla / Rodriguez, Anaelena / Yu, Connie / Nguyen, Lisa / Liang, Olin / Chorzalska, Anna / Dubielecka, Patrycja M

    Cell communication and signaling : CCS

    2023  Volume 21, Issue 1, Page(s) 291

    Abstract: NF-κB transcription factors are critical regulators of innate and adaptive immunity and major mediators of inflammatory signaling. The NF-κB signaling is dysregulated in a significant number of cancers and drives malignant transformation through ... ...

    Abstract NF-κB transcription factors are critical regulators of innate and adaptive immunity and major mediators of inflammatory signaling. The NF-κB signaling is dysregulated in a significant number of cancers and drives malignant transformation through maintenance of constitutive pro-survival signaling and downregulation of apoptosis. Overactive NF-κB signaling results in overexpression of pro-inflammatory cytokines, chemokines and/or growth factors leading to accumulation of proliferative signals together with activation of innate and select adaptive immune cells. This state of chronic inflammation is now thought to be linked to induction of malignant transformation, angiogenesis, metastasis, subversion of adaptive immunity, and therapy resistance. Moreover, accumulating evidence indicates the involvement of NF-κB signaling in induction and maintenance of invasive phenotypes linked to epithelial to mesenchymal transition (EMT) and metastasis. In this review we summarize reported links of NF-κB signaling to sequential steps of transition from epithelial to mesenchymal phenotypes. Understanding the involvement of NF-κB in EMT regulation may contribute to formulating optimized therapeutic strategies in cancer. Video Abstract.
    MeSH term(s) Humans ; NF-kappa B/metabolism ; Epithelial-Mesenchymal Transition/genetics ; Signal Transduction ; Neoplasms/metabolism ; Cell Transformation, Neoplastic ; Phenotype ; Cell Line, Tumor
    Chemical Substances NF-kappa B
    Language English
    Publishing date 2023-10-18
    Publishing country England
    Document type Video-Audio Media ; Journal Article ; Review ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
    ZDB-ID 2126315-2
    ISSN 1478-811X ; 1478-811X
    ISSN (online) 1478-811X
    ISSN 1478-811X
    DOI 10.1186/s12964-023-01207-z
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article: Murine Leukemia-Derived Extracellular Vesicles Elicit Antitumor Immune Response.

    Pando, Alejandro / Fast, Loren / Dubielecka, Patrycja M / Chorzalska, Anna / Wen, Sicheng / Reagan, John

    Journal of blood medicine

    2021  Volume 12, Page(s) 277–285

    Abstract: Background: Extracellular vesicles (EVs) are heterogeneous lipid bilayer particles secreted by cells. EVs contain proteins, RNA, DNA and other cargo that can have immunomodulatory effects. Cancer-derived EVs have been described as having ... ...

    Abstract Background: Extracellular vesicles (EVs) are heterogeneous lipid bilayer particles secreted by cells. EVs contain proteins, RNA, DNA and other cargo that can have immunomodulatory effects. Cancer-derived EVs have been described as having immunomodulating effects in vivo with immunosuppressive and pro-tumor growth capabilities. However, cancer-derived EVs have also been harnessed and utilized for anti-cancer potential.
    Methods: To assess the immunomodulatory effect of EVs produced by acute myeloid leukemia (AML) cells, we isolated vesicles secreted by the murine AML cell line, C1498, and investigated their effect on in vitro and in vivo immune responses.
    Results: These leukemia-derived EVs were found to induce increased proliferation of CD3+ cells and enhanced cytolytic activity of CD3+ cells directed toward leukemic cells in vitro. Injection of leukemia-derived EVs into syngeneic naïve mice induced T cell responses in vivo and resulted in enhanced immune responses upon T cell re-stimulation in vitro.
    Conclusion: These findings indicate that C1498-derived EVs have immunomodulatory effects on cell-mediated immune responses that could potentially be utilized to facilitate anti-leukemia immune responses.
    Language English
    Publishing date 2021-05-17
    Publishing country New Zealand
    Document type Journal Article
    ZDB-ID 2587464-0
    ISSN 1179-2736
    ISSN 1179-2736
    DOI 10.2147/JBM.S308861
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Proximity proteomics reveals role of Abelson interactor 1 in the regulation of TAK1/RIPK1 signaling.

    Petersen, Max / Chorzalska, Anna / Pardo, Makayla / Rodriguez, Anaelena / Morgan, John / Ahsan, Nagib / Zhao, Ting C / Liang, Olin / Kotula, Leszek / Bertone, Paul / Gruppuso, Philip A / Dubielecka, Patrycja M

    Molecular oncology

    2023  Volume 17, Issue 11, Page(s) 2356–2379

    Abstract: Dysregulation of the adaptor protein Abelson interactor 1 (ABI1) is linked to malignant transformation. To interrogate the role of ABI1 in cancer development, we mapped the ABI1 interactome using proximity-dependent labeling (PDL) with biotin followed by ...

    Abstract Dysregulation of the adaptor protein Abelson interactor 1 (ABI1) is linked to malignant transformation. To interrogate the role of ABI1 in cancer development, we mapped the ABI1 interactome using proximity-dependent labeling (PDL) with biotin followed by mass spectrometry. Using a novel PDL data filtering strategy, considering both peptide spectral matches and peak areas of detected peptides, we identified 212 ABI1 proximal interactors. These included WAVE2 complex components such as CYFIP1, NCKAP1, or WASF1, confirming the known role of ABI1 in the regulation of actin-polymerization-dependent processes. We also identified proteins associated with the TAK1-IKK pathway, including TAK1, TAB2, and RIPK1, denoting a newly identified function of ABI1 in TAK1-NF-κB inflammatory signaling. Functional assays using TNFα-stimulated, ABI1-overexpressing or ABI1-deficient cells showed effects on the TAK1-NF-kB pathway-dependent signaling to RIPK1, with ABI1-knockout cells being less susceptible to TNFα-induced, RIPK1-mediated, TAK1-dependent apoptosis. In sum, our PDL-based strategy enabled mapping of the ABI1 proximal interactome, thus revealing a previously unknown role of this adaptor protein in TAK1/RIPK1-based regulation of cell death and survival.
    MeSH term(s) Humans ; Tumor Necrosis Factor-alpha/pharmacology ; Tumor Necrosis Factor-alpha/metabolism ; Proteomics ; Signal Transduction ; NF-kappa B/metabolism ; Apoptosis/physiology ; Receptor-Interacting Protein Serine-Threonine Kinases/genetics ; Receptor-Interacting Protein Serine-Threonine Kinases/metabolism ; Adaptor Proteins, Signal Transducing/genetics ; Adaptor Proteins, Signal Transducing/metabolism ; Cytoskeletal Proteins/metabolism ; Wiskott-Aldrich Syndrome Protein Family/metabolism
    Chemical Substances Tumor Necrosis Factor-alpha ; NF-kappa B ; RIPK1 protein, human (EC 2.7.11.1) ; Receptor-Interacting Protein Serine-Threonine Kinases (EC 2.7.11.1) ; TAB2 protein, human ; Adaptor Proteins, Signal Transducing ; ABI1 protein, human ; Cytoskeletal Proteins ; WASF1 protein, human ; Wiskott-Aldrich Syndrome Protein Family
    Language English
    Publishing date 2023-05-12
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2415106-3
    ISSN 1878-0261 ; 1574-7891
    ISSN (online) 1878-0261
    ISSN 1574-7891
    DOI 10.1002/1878-0261.13374
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  4. Article: Engraftment, Fate, and Function of HoxB8-Conditional Neutrophil Progenitors in the Unconditioned Murine Host.

    Cohen, Joshua T / Danise, Michael / Hinman, Kristina D / Neumann, Brittany M / Johnson, Renita / Wilson, Zachary S / Chorzalska, Anna / Dubielecka, Patrycja M / Lefort, Craig T

    Frontiers in cell and developmental biology

    2022  Volume 10, Page(s) 840894

    Abstract: The development and use of murine myeloid progenitor cell lines that are conditionally immortalized through expression of HoxB8 has provided a valuable tool for studies of neutrophil biology. Recent work has extended the utility of HoxB8-conditional ... ...

    Abstract The development and use of murine myeloid progenitor cell lines that are conditionally immortalized through expression of HoxB8 has provided a valuable tool for studies of neutrophil biology. Recent work has extended the utility of HoxB8-conditional progenitors to the
    Language English
    Publishing date 2022-01-20
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2737824-X
    ISSN 2296-634X
    ISSN 2296-634X
    DOI 10.3389/fcell.2022.840894
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  5. Article ; Online: PKC-θ is a negative regulator of TRAIL-induced and FADD-mediated apoptotic spectrin aggregation.

    Michalczyk, Izabela / Toporkiewicz, Monika / Dubielecka, Patrycja M / Chorzalska, Anna / Sikorski, Aleksander F

    Folia histochemica et cytobiologica

    2016  Volume 54, Issue 1, Page(s) 1–13

    Abstract: Introduction: During studies on chemotherapy-induced apoptosis in lymphoid cells, we noted that aggregation of spectrin occurred early in apoptosis, i.e. before activation of initiator caspase(s) and prior to exposure of phosphatidylserine (PS). We also ...

    Abstract Introduction: During studies on chemotherapy-induced apoptosis in lymphoid cells, we noted that aggregation of spectrin occurred early in apoptosis, i.e. before activation of initiator caspase(s) and prior to exposure of phosphatidylserine (PS). We also found that protein kinase C theta (PKC-θ) co-localized with spectrin in these aggregates. Our previously published studies indicated that in formation of early apoptotic spectrin aggregates, either PKC-θ or other apoptosis-related proteins are involved. Taking into consideration above data, we decided to test the effect of PKC-θ and Fas-associated death domain protein (FADD) on spectrin aggregation in these cells during tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-induced apoptosis.
    Material and methods: For PKC-θ gene (PRKCQ) or FADD gene expression silencing in Jurkat T cells we used lentiviral particles containing shRNA and scrambled shRNA, respectively. Spectrin aggregates were detected by Western blotting after Triton-X 100 extraction in pellet and soluble fractions or by confocal imaging.
    Results: TRAIL-induced apoptosis results in spectrin aggregation and leads to translocation and aggregation of PKC-θ. We found that phorbol-myristate acetate, a PKC activator and translocation inducer, has only a small effect on spectrin aggregation. To further confirm this, we have also shown that knock down ofPRKCQin Jurkat T cells accelerates the formation of TRAIL-induced spectrin aggregates. Transient overexpression of theβ-spectrin C-terminal fragment, containing multiple S/T phosphorylation sites, potential substrate sites for PKC-θ, accelerated the formation of spectrin aggregates. Silencing of downstream TRAIL receptor effector gene,FADD, delayed aggregation of spectrin, but did not reduce PKC-θ localization to the plasma membrane.
    Conclusions: In summary, our results show for the first time involvement of spectrin aggregation in TRAIL receptor-FADD apoptotic pathway and indicate that TRAIL-induced spectrin aggregate formation is mediated by FADD and negatively regulated by PKC-θ.
    MeSH term(s) Apoptosis/drug effects ; Apoptosis/physiology ; Caspases/metabolism ; Cells, Cultured ; Down-Regulation/drug effects ; Fas-Associated Death Domain Protein/genetics ; Fas-Associated Death Domain Protein/metabolism ; Humans ; Isoenzymes/biosynthesis ; Isoenzymes/genetics ; Isoenzymes/metabolism ; Jurkat Cells ; Lymphocytes ; Phosphorylation ; Protein Kinase C/biosynthesis ; Protein Kinase C/genetics ; Protein Kinase C/metabolism ; Protein Kinase C-theta ; RNA, Small Interfering/administration & dosage ; RNA, Small Interfering/genetics ; Signal Transduction ; Spectrin/metabolism ; T-Lymphocytes/metabolism ; TNF-Related Apoptosis-Inducing Ligand/pharmacology ; Tetradecanoylphorbol Acetate/pharmacology
    Chemical Substances FADD protein, human ; Fas-Associated Death Domain Protein ; Isoenzymes ; RNA, Small Interfering ; TNF-Related Apoptosis-Inducing Ligand ; TNFSF10 protein, human ; Spectrin (12634-43-4) ; PRKCQ protein, human (EC 2.7.11.13) ; Protein Kinase C (EC 2.7.11.13) ; Protein Kinase C-theta (EC 2.7.11.13) ; Caspases (EC 3.4.22.-) ; Tetradecanoylphorbol Acetate (NI40JAQ945)
    Language English
    Publishing date 2016
    Publishing country Poland
    Document type Journal Article
    ZDB-ID 605761-5
    ISSN 1897-5631 ; 0015-5586 ; 0239-8508
    ISSN (online) 1897-5631
    ISSN 0015-5586 ; 0239-8508
    DOI 10.5603/FHC.a2016.0006
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Detection of clonotypic DNA in the cerebrospinal fluid as a marker of central nervous system invasion in lymphoma.

    Olszewski, Adam J / Chorzalska, Anna D / Petersen, Max / Ollila, Thomas A / Zayac, Adam / Kurt, Habibe / Treaba, Diana O / Reagan, John L / Hsu, Andrew / Egan, Pamela C / Butera, James / Niroula, Rabin / Vatkevich, John / Robison, Jordan / Sahin, Ilyas / Jacob, Allison P / Mullins, Chelsea D / Dubielecka, Patrycja M

    Blood advances

    2021  Volume 5, Issue 24, Page(s) 5525–5535

    Abstract: The diagnosis of parenchymal central nervous system (CNS) invasion and prediction of risk for future CNS recurrence are major challenges in the management of aggressive lymphomas, and accurate biomarkers are needed to supplement clinical risk predictors. ...

    Abstract The diagnosis of parenchymal central nervous system (CNS) invasion and prediction of risk for future CNS recurrence are major challenges in the management of aggressive lymphomas, and accurate biomarkers are needed to supplement clinical risk predictors. For this purpose, we studied the results of a next-generation sequencing (NGS)-based assay that detects tumor-derived DNA for clonotypic immunoglobulin gene rearrangements in the cerebrospinal fluid (CSF) of patients with lymphomas. Used as a diagnostic tool, the NGS-minimal residual disease (NGS-MRD) assay detected clonotypic DNA in 100% of CSF samples from 13 patients with known CNS involvement. They included 7 patients with parenchymal brain disease only, whose CSF tested negative by standard cytology and flow cytometry, and 6 historical DNA aliquots collected from patients at a median of 39 months before accession, which had failed to show clonal rearrangements using standard polymerase chain reaction. For risk prognostication, we prospectively collected CSF from 22 patients with newly diagnosed B-cell lymphomas at high clinical risk of CNS recurrence, of whom 8 (36%) had detectable clonotypic DNA in the CSF. Despite intrathecal prophylaxis, a positive assay of CSF was associated with a 29% cumulative risk of CNS recurrence within 12 months of diagnosis, in contrast with a 0% risk among patients with negative CSF (P = .045). These observations suggest that detection of clonotypic DNA can aid in the diagnosis of suspected parenchymal brain recurrence in aggressive lymphoma. Furthermore, the NGS-MRD assay may enhance clinical risk assessment for CNS recurrence among patients with newly diagnosed lymphomas and help select those who may benefit most from novel approaches to CNS-directed prophylaxis.
    MeSH term(s) Biomarkers ; Central Nervous System ; DNA ; Humans ; Lymphoma, B-Cell ; Lymphoma, Non-Hodgkin
    Chemical Substances Biomarkers ; DNA (9007-49-2)
    Language English
    Publishing date 2021-09-20
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2915908-8
    ISSN 2473-9537 ; 2473-9529
    ISSN (online) 2473-9537
    ISSN 2473-9529
    DOI 10.1182/bloodadvances.2021004512
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  7. Article ; Online: Transcriptomics of acute myeloid leukaemia core bone marrow biopsies reveals distinct therapy response-specific osteo-mesenchymal profiles.

    Treaba, Diana O / Bonal, Dennis M / Chorzalska, Anna / Castillo-Martin, Mireia / Oakes, Alissa / Pardo, Makayla / Petersen, Max / Schorl, Christoph / Hopkins, Kelsey / Melcher, Dean / Zhao, Ting C / Liang, Olin / So, Eui-Young / Reagan, John / Olszewski, Adam J / Butera, James / Anthony, Douglas C / Rintels, Peter / Quesenberry, Peter /
    Dubielecka, Patrycja M

    British journal of haematology

    2022  Volume 200, Issue 6, Page(s) 740–754

    Abstract: While the bone marrow (BM) microenvironment is significantly remodelled in acute myeloid leukaemia (AML), molecular insight into AML-specific alterations in the microenvironment has been historically limited by the analysis of liquid marrow aspirates ... ...

    Abstract While the bone marrow (BM) microenvironment is significantly remodelled in acute myeloid leukaemia (AML), molecular insight into AML-specific alterations in the microenvironment has been historically limited by the analysis of liquid marrow aspirates rather than core biopsies that contain solid-phase BM stroma. We assessed the effect of anthracycline- and cytarabine-based induction chemotherapy on both haematopoietic and non-haematopoietic cells directly in core BM biopsies using RNA-seq and histological analysis. We compared matched human core BM biopsies at diagnosis and 2 weeks after cytarabine- and anthracycline-based induction therapy in responders (<5% blasts present after treatment) and non-responders (≥5% blasts present after treatment). Our data indicated enrichment in vimentin (VIM), platelet-derived growth factor receptor beta (PDGFRB) and Snail family transcriptional repressor 2 (SNAI2) transcripts in responders, consistent with the reactivation of the mesenchymal population in the BM stroma. Enrichment of osteoblast maturation-related transcripts of biglycan (BGN), osteopontin (SPP1) and osteonectin (SPARC) was observed in non-responders. To the best of our knowledge, this is the first report demonstrating distinct osteogenic and mesenchymal transcriptome profiles specific to AML response to induction chemotherapy assessed directly in core BM biopsies. Detailing treatment response-specific alterations in the BM stroma may inform optimised therapeutic strategies for AML.
    MeSH term(s) Humans ; Bone Marrow/pathology ; Transcriptome ; Leukemia, Myeloid, Acute/drug therapy ; Cytarabine/therapeutic use ; Bone Marrow Cells/pathology ; Anthracyclines/therapeutic use ; Biopsy ; Tumor Microenvironment
    Chemical Substances Cytarabine (04079A1RDZ) ; Anthracyclines
    Language English
    Publishing date 2022-11-10
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 80077-6
    ISSN 1365-2141 ; 0007-1048
    ISSN (online) 1365-2141
    ISSN 0007-1048
    DOI 10.1111/bjh.18513
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  8. Article ; Online: Clonal haematopoiesis of indeterminate potential among cancer survivors exposed to myelotoxic chemotherapy.

    Olszewski, Adam J / Chorzalska, Anna D / Kim, Annette S / Quesenberry, Peter J / Lopresti, Mary L / Fenton, Mary A / Reagan, John L / Butera, James N / Sahin, Ilyas / Hamel, Celine / Robison, Jordan / Petersen, Max / Dubielecka, Patrycja M

    British journal of haematology

    2019  Volume 186, Issue 3, Page(s) e31–e35

    MeSH term(s) Aged ; Cancer Survivors ; Clonal Evolution ; Female ; Hematopoiesis/physiology ; Humans ; Male ; Middle Aged ; Neoplasms/blood ; Neoplasms/drug therapy ; Neoplasms/genetics ; Neoplasms/mortality
    Language English
    Publishing date 2019-03-11
    Publishing country England
    Document type Letter ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 80077-6
    ISSN 1365-2141 ; 0007-1048
    ISSN (online) 1365-2141
    ISSN 0007-1048
    DOI 10.1111/bjh.15861
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  9. Article ; Online: The 22.5 kDa spectrin-binding domain of ankyrinR binds spectrin with high affinity and changes the spectrin distribution in cells in vivo.

    Kolondra, Adam / Grzybek, Michal / Chorzalska, Anna / Sikorski, Aleksander F

    Protein expression and purification

    2008  Volume 60, Issue 2, Page(s) 157–164

    Abstract: It was previously shown that ankyrins play a crucial role in the membrane skeleton arrangement. Purifying ankyrinR obtained from erythrocytes is a time-consuming process. Therefore, cloned and bacterially expressed ankyrinR-spectrin-binding domain ( ... ...

    Abstract It was previously shown that ankyrins play a crucial role in the membrane skeleton arrangement. Purifying ankyrinR obtained from erythrocytes is a time-consuming process. Therefore, cloned and bacterially expressed ankyrinR-spectrin-binding domain (AnkSBD) is a demanded tool for studying spectrin-ankyrin interactions. In this communication, we report on the cloning and purification of AnkSBD and describe the results of binding experiments, in which we showed high-affinity interactions between the AnkSBD construct and isolated erythrocyte or non-erythroid spectrins. pEGFP-AnkSBD-transfected cells co-localised with non-erythroid spectrin in HeLa cells. The functional interactions of the AnkSBD construct in vivo and in vitro open many possibilities to study the structure and function of this domain, which has not yet been as extensively studied when compared to the aminoterminal domain of this protein.
    MeSH term(s) Ankyrins/genetics ; Ankyrins/isolation & purification ; Ankyrins/metabolism ; Base Sequence ; Chromatography, Affinity ; Cloning, Molecular ; DNA Primers ; DNA, Complementary ; Electrophoresis, Polyacrylamide Gel ; Escherichia coli/genetics ; HeLa Cells ; Humans ; Microscopy, Fluorescence ; Plasmids ; Polymerase Chain Reaction ; Protein Binding ; Spectrin/genetics ; Spectrin/isolation & purification ; Spectrin/metabolism
    Chemical Substances Ankyrins ; DNA Primers ; DNA, Complementary ; Spectrin (12634-43-4)
    Language English
    Publishing date 2008-08
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1055455-5
    ISSN 1096-0279 ; 1046-5928
    ISSN (online) 1096-0279
    ISSN 1046-5928
    DOI 10.1016/j.pep.2008.04.002
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  10. Article ; Online: Overexpression of Tpl2 is linked to imatinib resistance and activation of MEK-ERK and NF-κB pathways in a model of chronic myeloid leukemia.

    Chorzalska, Anna / Ahsan, Nagib / Rao, R Shyama Prasad / Roder, Karim / Yu, Xiaoqing / Morgan, John / Tepper, Alexander / Hines, Steven / Zhang, Peng / Treaba, Diana O / Zhao, Ting C / Olszewski, Adam J / Reagan, John L / Liang, Olin / Gruppuso, Philip A / Dubielecka, Patrycja M

    Molecular oncology

    2018  Volume 12, Issue 5, Page(s) 630–647

    Abstract: The introduction of tyrosine kinase inhibitors (TKI) has transformed chronic myeloid leukemia (CML) into a chronic disease with long-term survival exceeding 85%. However, resistance of CML stem cells to TKI may contribute to the 50% relapse rate observed ...

    Abstract The introduction of tyrosine kinase inhibitors (TKI) has transformed chronic myeloid leukemia (CML) into a chronic disease with long-term survival exceeding 85%. However, resistance of CML stem cells to TKI may contribute to the 50% relapse rate observed after TKI discontinuation in molecular remission. We previously described a model of resistance to imatinib mesylate (IM), in which K562 cells cultured in high concentrations of imatinib mesylate showed reduced Bcr-Abl1 protein and activity levels while maintaining proliferative potential. Using quantitative phosphoproteomic analysis of these IM-resistant cells, we have now identified significant upregulation of tumor progression locus (Tpl2), also known as cancer Osaka thyroid (COT1) kinase or Map3k8. Overexpression of Tpl2 in IM-resistant cells was accompanied by elevated activities of Src family kinases (SFKs) and NF-κB, MEK-ERK signaling. CD34+ cells isolated from the bone marrow of patients with CML and exposed to IMin vitro showed increased MAP3K8 transcript levels. Dasatinib (SFK inhibitor), U0126 (MEK inhibitor), and PS-1145 (IκB kinase (IKK) inhibitor) used in combination resulted in elimination of 65% of IM-resistant cells and reduction in the colony-forming capacity of CML CD34+ cells in methylcellulose assays by 80%. In addition, CML CD34+ cells cultured with the combination of inhibitors showed reduced MAP3K8 transcript levels. Overall, our data indicate that elevated Tpl2 protein and transcript levels are associated with resistance to IM and that combined inhibition of SFK, MEK, and NF-κB signaling attenuates the survival of IM-resistant CML cells and CML CD34+ cells. Therefore, combination of SFK, MEK, and NF-κB inhibitors may offer a new therapeutic approach to overcome TKI resistance in CML patients.
    MeSH term(s) Animals ; Cell Line, Tumor ; Disease Models, Animal ; Drug Resistance, Neoplasm ; Fusion Proteins, bcr-abl/metabolism ; Humans ; Imatinib Mesylate/pharmacology ; Imatinib Mesylate/therapeutic use ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive/metabolism ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive/pathology ; MAP Kinase Kinase Kinases/metabolism ; MAP Kinase Signaling System ; Mitogen-Activated Protein Kinase Kinases/metabolism ; Models, Biological ; NF-kappa B/metabolism ; Phosphopeptides/metabolism ; Proteomics ; Proto-Oncogene Proteins/metabolism ; Signal Transduction ; src-Family Kinases/metabolism
    Chemical Substances NF-kappa B ; Phosphopeptides ; Proto-Oncogene Proteins ; Imatinib Mesylate (8A1O1M485B) ; Fusion Proteins, bcr-abl (EC 2.7.10.2) ; src-Family Kinases (EC 2.7.10.2) ; MAP Kinase Kinase Kinases (EC 2.7.11.25) ; MAP3K8 protein, human (EC 2.7.11.25) ; Mitogen-Activated Protein Kinase Kinases (EC 2.7.12.2)
    Language English
    Publishing date 2018-04-06
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2415106-3
    ISSN 1878-0261 ; 1574-7891
    ISSN (online) 1878-0261
    ISSN 1574-7891
    DOI 10.1002/1878-0261.12186
    Database MEDical Literature Analysis and Retrieval System OnLINE

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