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Article ; Online: Geohash-Based Rapid Query Method of Regional Transactions in Blockchain for Internet of Vehicles.

Zhou, Chang / Lu, Huimei / Xiang, Yong / Wu, Jingbang / Wang, Feng

2022 Volume 22, Issue 22

Abstract: Many researchers have introduced blockchain into the Internet of Vehicles (IoV) to support trading or other authentication applications between vehicles. However, the traditional blockchain cannot well support the query of transactions that occur in a ... ...

Abstract	Many researchers have introduced blockchain into the Internet of Vehicles (IoV) to support trading or other authentication applications between vehicles. However, the traditional blockchain cannot well support the query of transactions that occur in a specified area which is important for vehicle users since they are bound to the geolocations. Therefore, the querying efficiency of the geolocation attribute of transactions is vital for blockchain-based applications. Existing work does not well handle the geolocation of vehicles in the blockchain, and thus the querying efficiency is questionable. In this paper, we design a rapid query method of regional transactions in blockchain for IoV, including data structures and query algorithms. The main idea is to utilize the Geohash code to represent the area and serve as the key for transaction indexing and querying, and the geolocation is marked as one of the attributes of transactions in the blockchain. To further verify and evaluate the proposed design, on the basis of the implementation of Ethereum, which is a well-known blockchain, the results show that the proposed design achieves significantly better-querying speed than Ethereum.
MeSH term(s)	Blockchain ; Computer Security ; Internet ; Algorithms
Language	English
Publishing date	2022-11-17
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2052857-7
ISSN	1424-8220 ; 1424-8220
ISSN (online)	1424-8220
ISSN	1424-8220
DOI	10.3390/s22228885
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Article ; Online: SETD4-mediated KU70 methylation suppresses apoptosis.

Wang, Yuan / Liu, Bochao / Lu, Huimei / Liu, Jingmei / Romanienko, Peter J / Montelione, Gaetano T / Shen, Zhiyuan

Cell reports

2022 Volume 39, Issue 6, Page(s) 110794

Abstract: The mammalian KU70 is a pleiotropic protein functioning in DNA repair and cytoplasmic suppression of apoptosis. We report a regulatory mechanism by which KU70's cytoplasmic function is enabled due to a methylation at K570 of KU70 by SET-domain-containing ...

Abstract	The mammalian KU70 is a pleiotropic protein functioning in DNA repair and cytoplasmic suppression of apoptosis. We report a regulatory mechanism by which KU70's cytoplasmic function is enabled due to a methylation at K570 of KU70 by SET-domain-containing protein 4 (SETD4). While SETD4 silencing reduces the level of methylated KU70, over-expression of SETD4 enhances methylation of KU70. Mutations of Y272 and Y284 of SETD4 abrogate methylation of KU70. Although SETD4 is predominantly a nuclear protein, the methylated KU70 is enriched in the cytoplasm. SETD4 knockdown enhances staurosporine (STS)-induced apoptosis and cell killing. Over-expression of the wild-type (WT) SETD4, but not the SETD4-Y272/Y284F mutant, suppresses STS-induced apoptosis. The KU70-K570R (mouse Ku70-K568R) mutation dampens the anti-apoptosis activity of KU70. Our study identifies KU70 as a non-histone substrate of SETD4, discovers a post-translational modification of KU70, and uncovers a role for SETD4 and KU70-K570 methylation in the suppression of apoptosis.
MeSH term(s)	Animals ; Antigens, Nuclear/genetics ; Antigens, Nuclear/metabolism ; Apoptosis/genetics ; Cytoplasm/metabolism ; DNA Repair ; Ku Autoantigen/genetics ; Ku Autoantigen/metabolism ; Mammals/metabolism ; Methylation ; Methyltransferases ; Mice ; Protein Processing, Post-Translational
Chemical Substances	Antigens, Nuclear ; Methyltransferases (EC 2.1.1.-) ; Setd4 protein, mouse (EC 2.1.1.-) ; Xrcc6 protein, mouse (EC 3.6.4.12) ; Ku Autoantigen (EC 4.2.99.-)
Language	English
Publishing date	2022-05-11
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	2649101-1
ISSN	2211-1247 ; 2211-1247
ISSN (online)	2211-1247
ISSN	2211-1247
DOI	10.1016/j.celrep.2022.110794
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Article ; Online: BCCIP is required for nucleolar recruitment of eIF6 and 12S pre-rRNA production during 60S ribosome biogenesis.

Ye, Caiyong / Liu, Bochao / Lu, Huimei / Liu, Jingmei / Rabson, Arnold B / Jacinto, Estela / Pestov, Dimitri G / Shen, Zhiyuan

Nucleic acids research

2021 Volume 48, Issue 22, Page(s) 12817–12832

Abstract: Ribosome biogenesis is a fundamental process required for cell proliferation. Although evolutionally conserved, the mammalian ribosome assembly system is more complex than in yeasts. BCCIP was originally identified as a BRCA2 and p21 interacting protein. ...

Abstract	Ribosome biogenesis is a fundamental process required for cell proliferation. Although evolutionally conserved, the mammalian ribosome assembly system is more complex than in yeasts. BCCIP was originally identified as a BRCA2 and p21 interacting protein. A partial loss of BCCIP function was sufficient to trigger genomic instability and tumorigenesis. However, a complete deletion of BCCIP arrested cell growth and was lethal in mice. Here, we report that a fraction of mammalian BCCIP localizes in the nucleolus and regulates 60S ribosome biogenesis. Both abrogation of BCCIP nucleolar localization and impaired BCCIP-eIF6 interaction can compromise eIF6 recruitment to the nucleolus and 60S ribosome biogenesis. BCCIP is vital for a pre-rRNA processing step that produces 12S pre-rRNA, a precursor to the 5.8S rRNA. However, a heterozygous Bccip loss was insufficient to impair 60S biogenesis in mouse embryo fibroblasts, but a profound reduction of BCCIP was required to abrogate its function in 60S biogenesis. These results suggest that BCCIP is a critical factor for mammalian pre-rRNA processing and 60S generation and offer an explanation as to why a subtle dysfunction of BCCIP can be tumorigenic but a complete depletion of BCCIP is lethal.
MeSH term(s)	Animals ; BRCA2 Protein/genetics ; Carcinogenesis/genetics ; Cell Cycle Proteins/genetics ; Cell Proliferation/genetics ; Cyclin-Dependent Kinase Inhibitor p21/genetics ; Eukaryotic Initiation Factors/genetics ; Fibroblasts ; Genomic Instability/genetics ; Humans ; Mice ; NIH 3T3 Cells ; Protein Interaction Maps/genetics ; RNA, Ribosomal/genetics ; RNA, Ribosomal, 5.8S/genetics ; Ribosome Subunits, Large, Eukaryotic/genetics ; Ribosomes/genetics
Chemical Substances	BCCIP protein, mouse ; BRCA2 Protein ; BRCA2 protein, human ; CDKN1A protein, human ; Cell Cycle Proteins ; Cyclin-Dependent Kinase Inhibitor p21 ; EIF6 protein, human ; Eukaryotic Initiation Factors ; RNA, Ribosomal ; RNA, Ribosomal, 5.8S ; RNA, ribosomal, 12S
Language	English
Publishing date	2021-01-03
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	186809-3
ISSN	1362-4962 ; 1362-4954 ; 0301-5610 ; 0305-1048
ISSN (online)	1362-4962 ; 1362-4954
ISSN	0301-5610 ; 0305-1048
DOI	10.1093/nar/gkaa1114
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Article ; Online: Deletion of Mouse Setd4 Promotes the Recovery of Hematopoietic Failure.

Feng, Xing / Lu, Huimei / Yue, Jingyin / Shettigar, Megha / Liu, Jingmei / Denzin, Lisa K / Shen, Zhiyuan

International journal of radiation oncology, biology, physics

2020 Volume 107, Issue 4, Page(s) 779–792

Abstract: Purpose: Acquired hematopoietic failure is commonly caused by therapeutic and accidental exposure of the bone marrow (BM) to toxic agents. Efficient recovery from BM failure is dictated not only by the intrinsic sensitivity and proliferation capacity of ...

Abstract	Purpose: Acquired hematopoietic failure is commonly caused by therapeutic and accidental exposure of the bone marrow (BM) to toxic agents. Efficient recovery from BM failure is dictated not only by the intrinsic sensitivity and proliferation capacity of the hematopoietic stem and progenitor cells but also by the BM environment niche. Identification of genetic factors that improve recovery from hematopoietic failure is essential. Vertebrate SETD4 is a poorly characterized and putatively nonhistone methyltransferase. This study aims to identify the roles of SETD4 in BM recovery. Methods and materials: An inducible SETD4 knockout mouse model (Setd4 Results: Loss of Setd4 in adult mice improved the survival of whole-body irradiation-induced BM failure. This was associated with improved recoveries of long-term and short-term hematopoietic stem cells (HSCs) and early progenitor cells. BM transplantation analyses surprisingly showed that the improved recovery was not due to radiation resistance of the Setd4-deficient HSCs but that Setd4-deficient HSCs were actually more sensitive to radiation. However, the Setd4-deficient mice were better recipients for allogeneic HSC transplantation. Furthermore, there was enhanced splenic erythropoiesis in Setd4-deficient mice. Conclusion: These findings not only revealed a previously unrecognized role of Setd4 as a unique modulator of hematopoiesis but also underscored the critical role of the BM niche in recovery from hematopoietic failure. Our study also implicated Setd4 as a potential target for therapeutic inhibition to improve the conditioning of the BM niche before allogeneic transplantation.
MeSH term(s)	Animals ; Bone Marrow Transplantation ; Gene Knockout Techniques ; Hematopoiesis/genetics ; Hematopoiesis/radiation effects ; Methyltransferases/deficiency ; Methyltransferases/genetics ; Mice ; Whole-Body Irradiation/adverse effects
Chemical Substances	Methyltransferases (EC 2.1.1.-) ; Setd4 protein, mouse (EC 2.1.1.-)
Language	English
Publishing date	2020-04-04
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	197614-x
ISSN	1879-355X ; 0360-3016
ISSN (online)	1879-355X
ISSN	0360-3016
DOI	10.1016/j.ijrobp.2020.03.026
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Article ; Online: Requirement of Bccip for the Regeneration of Intestinal Progenitors.

Lu, Huimei / Ye, Caiyong / Liu, Jingmei / Rabson, Arnold B / Verzi, Michael / De, Subhajyoti / Shen, Zhiyuan

The American journal of pathology

2020 Volume 191, Issue 1, Page(s) 66–78

Abstract: BCCIP was originally identified as a BRCA2 and CDKN1A/p21 interaction protein. Although a partial loss of BCCIP function is sufficient to trigger genomic instability and tumorigenesis, complete deletion of BCCIP is lethal to cells. Using Rosa26-CreERT2 ... ...

Abstract	BCCIP was originally identified as a BRCA2 and CDKN1A/p21 interaction protein. Although a partial loss of BCCIP function is sufficient to trigger genomic instability and tumorigenesis, complete deletion of BCCIP is lethal to cells. Using Rosa26-CreERT2 mouse models, we found that induced Bccip deletion in adult mice caused an acute intestinal epithelial denudation that cannot be relieved by co-deletion of Trp53. The critical role of Bccip in intestine epithelial renewal was verified with a Villin-CreERT2 mouse model. The epithelium degeneration was associated with a rapid loss of the proliferative capability of the crypt progenitor cells in vivo, lack of crypt base columnar stem cell markers, and a failure of in vitro crypt organoid growth. RNA-Seq analysis of freshly isolated intestinal crypt cells showed that Bccip deletion caused an overwhelming down-regulation of genes involved in mitotic cell division but an up-regulation of genes involved in apoptosis and stress response to microbiomes. Our data not only indicate that intestinal epithelium is the most sensitive tissue to whole-body deletion of Bccip but also point to Bccip as a novel and critical factor for the proliferation of the intestinal progenitors. These findings have significant implications for understanding why a hypomorphic loss of BCCIP functions is more relevant to tumorigenesis.
MeSH term(s)	Animals ; Cell Cycle Proteins/metabolism ; Cell Proliferation/physiology ; Intestinal Mucosa/metabolism ; Mice ; Regeneration/physiology ; Stem Cells/metabolism
Chemical Substances	BCCIP protein, mouse ; Cell Cycle Proteins
Language	English
Publishing date	2020-10-09
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2943-9
ISSN	1525-2191 ; 0002-9440
ISSN (online)	1525-2191
ISSN	0002-9440
DOI	10.1016/j.ajpath.2020.09.009
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Article ; Online: Spontaneous Development of Hepatocellular Carcinoma and B-Cell Lymphoma in Mosaic and Heterozygous Brca2 and Cdkn1a Interacting Protein Knockout Mice.

Lu, Huimei / Ye, Caiyong / Feng, Xing / Liu, Jingmei / Bhaumik, Mantu / Xia, Bing / Liu, Chen / Shen, Zhiyuan

The American journal of pathology

2020 Volume 190, Issue 6, Page(s) 1175–1187

Abstract: Hepatocellular carcinoma (HCC) is the most common form of liver tumors. Although HCC is associated with chronic viral infections, alcoholic cirrhosis, and nonalcoholic fatty liver disease, genetic factors that contribute to the HCC risk remain unknown. ... ...

Abstract	Hepatocellular carcinoma (HCC) is the most common form of liver tumors. Although HCC is associated with chronic viral infections, alcoholic cirrhosis, and nonalcoholic fatty liver disease, genetic factors that contribute to the HCC risk remain unknown. The BRCA2 DNA repair associated (BRCA2) and cyclin-dependent kinase inhibitor 1A (CDKN1A) interacting protein, known as BCCIP, are essential for cell viability and maintenance of genomic stability. In this study, we established a new genetically engineered mouse model with Bccip deficiency. Mosaic or heterozygous Bccip deletion conferred an increased risk of spontaneous liver tumorigenesis and B-cell lymphoma development at old age. These abnormalities are accompanied with chronic inflammation, histologic features of nonalcoholic steatohepatitis, keratin and ubiquitin aggregates within cytoplasmic Mallory-Denk bodies, and changes of the intracellular distribution of high-mobility group box 1 protein. Our study suggests BCCIP dysregulation as a risk factor for HCC and offers a novel mouse model for future investigations of nonviral or nonalcoholic causes of HCC development.
MeSH term(s)	Animals ; BRCA2 Protein/genetics ; BRCA2 Protein/metabolism ; Carcinoma, Hepatocellular/genetics ; Carcinoma, Hepatocellular/metabolism ; Carcinoma, Hepatocellular/pathology ; Cell Cycle Proteins/genetics ; Cell Cycle Proteins/metabolism ; Heterozygote ; Liver Neoplasms/genetics ; Liver Neoplasms/metabolism ; Liver Neoplasms/pathology ; Lymphoma, B-Cell/genetics ; Lymphoma, B-Cell/metabolism ; Lymphoma, B-Cell/pathology ; Mice ; Mice, Knockout ; Mosaicism
Chemical Substances	BCCIP protein, mouse ; BRCA2 Protein ; Cell Cycle Proteins
Language	English
Publishing date	2020-03-20
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2943-9
ISSN	1525-2191 ; 0002-9440
ISSN (online)	1525-2191
ISSN	0002-9440
DOI	10.1016/j.ajpath.2020.01.020
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Article ; Online: Loss of Setd4 delays radiation-induced thymic lymphoma in mice.

Feng, Xing / Lu, Huimei / Yue, Jingyin / Schneider, Neta / Liu, Jingmei / Denzin, Lisa K / Chan, Chang S / De, Subhajyoti / Shen, Zhiyuan

DNA repair

2019 Volume 86, Page(s) 102754

Abstract: Radiation-induced lymphomagenesis results from a clonogenic lymphoid cell proliferation due to genetic alterations and immunological dysregulation. Mouse models had been successfully used to identify risk and protective factors for radiation-induced DNA ... ...

Abstract	Radiation-induced lymphomagenesis results from a clonogenic lymphoid cell proliferation due to genetic alterations and immunological dysregulation. Mouse models had been successfully used to identify risk and protective factors for radiation-induced DNA damage and carcinogenesis. The mammalian SETD4 is a poorly understood putative methyl-transferase. Here, we report that conditional Setd4 deletion in adult mice significantly extended the survival of radiation-induced T-lymphoma. However, in Tp53 deficient mice, Setd4 deletion did not delay the radiation-induced lymphomagenesis although it accelerated the spontaneous T-lymphomagenesis in non-irradiated mice. The T-lymphomas were largely clonogenic in both Setd4
MeSH term(s)	Animals ; CD4-Positive T-Lymphocytes/metabolism ; CD8-Positive T-Lymphocytes/metabolism ; Disease Models, Animal ; Gene Deletion ; Lymphoma/genetics ; Lymphoma/immunology ; Lymphoma/mortality ; Methyltransferases/genetics ; Mice ; Neoplasms, Radiation-Induced/genetics ; Neoplasms, Radiation-Induced/immunology ; Neoplasms, Radiation-Induced/mortality ; Receptors, Antigen, T-Cell, alpha-beta/genetics ; Sequence Analysis, DNA ; Thymus Neoplasms/genetics ; Thymus Neoplasms/immunology ; Thymus Neoplasms/mortality ; Tumor Suppressor Protein p53/genetics
Chemical Substances	Receptors, Antigen, T-Cell, alpha-beta ; Trp53 protein, mouse ; Tumor Suppressor Protein p53 ; Methyltransferases (EC 2.1.1.-) ; Setd4 protein, mouse (EC 2.1.1.-)
Language	English
Publishing date	2019-11-25
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2071608-4
ISSN	1568-7856 ; 1568-7864
ISSN (online)	1568-7856
ISSN	1568-7864
DOI	10.1016/j.dnarep.2019.102754
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Article ; Online: Roles of BCCIP deficiency in mammary tumorigenesis.

Droz-Rosario, Roberto / Lu, Huimei / Liu, Jingmei / Liu, Ning-Ang / Ganesan, Shridar / Xia, Bing / Haffty, Bruce G / Shen, Zhiyuan

Breast cancer research : BCR

2017 Volume 19, Issue 1, Page(s) 115

Abstract: Background: Dysregulated DNA repair and cell proliferation controls are essential driving forces in mammary tumorigenesis. BCCIP was originally identified as a BRCA2 and CDKN1A interacting protein that has been implicated in maintenance of genomic ... ...

Abstract	Background: Dysregulated DNA repair and cell proliferation controls are essential driving forces in mammary tumorigenesis. BCCIP was originally identified as a BRCA2 and CDKN1A interacting protein that has been implicated in maintenance of genomic stability, cell cycle regulation, and microtubule dynamics. The aims of this study were to determine whether BCCIP deficiency contributes to mammary tumorigenesis, especially for a subset of breast cancers with 53BP1 abnormality, and to reveal the mechanistic implications of BCCIP in breast cancer interventions. Methods: We analyzed the BCCIP protein level in 470 cases of human breast cancer to determine the associations between BCCIP and 53BP1, p53, and subtypes of breast cancer. We further constructed a unique BCCIP knockdown mouse model to determine whether a partial BCCIP deficiency leads to spontaneous breast cancer formation. Results: We found that the BCCIP protein level is downregulated in 49% of triple-negative breast cancer and 25% of nontriple-negative breast cancer. The downregulation of BCCIP is mutually exclusive with p53 mutations but concurrent with 53BP1 loss in triple-negative breast cancer. In a K14-Cre-mediated conditional BCCIP knockdown mouse model, we found that BCCIP downregulation causes a formation of benign modules in the mammary glands, resembling the epidermal inclusion cyst of the breast. However, the majority of these benign lesions remain indolent, and only ~ 10% of them evolve into malignant tumors after a long latency. This tumor progression is associated with a loss of 53BP1 and p16 expression. BCCIP knockdown did not alter the latency of mammary tumor formation induced by conditional Trp53 deletion. Conclusions: Our data suggest a confounding role of BCCIP deficiency in modulating breast cancer development by enhancing tumor initiation but hindering progression. Furthermore, secondary genetic alternations may overcome the progression suppression imposed by BCCIP deficiency through a synthetic viability mechanism.
Language	English
Publishing date	2017-10-18
Publishing country	England
Document type	Journal Article
ZDB-ID	2015059-3
ISSN	1465-542X ; 1465-5411
ISSN (online)	1465-542X
ISSN	1465-5411
DOI	10.1186/s13058-017-0907-5
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Article ; Online: Alterations of BCCIP, a BRCA2 interacting protein, in astrocytomas

Merlo Adrian / Ohgaki Hiroko / Lu Huimei / Liu Jingmei / Shen Zhiyuan

BMC Cancer, Vol 9, Iss 1, p

2009 Volume 268

Abstract: Abstract Background Loss of heterozygosity of chromosome 10q26 has been shown to be associated with the aggressiveness of astrocytic tumors (or astrocytomas), but the responsible gene(s) residing in this region has not been fully identified. The BCCIP ... ...

Abstract	Abstract Background Loss of heterozygosity of chromosome 10q26 has been shown to be associated with the aggressiveness of astrocytic tumors (or astrocytomas), but the responsible gene(s) residing in this region has not been fully identified. The BCCIP gene is located at chromosome 10q26. It encodes a BRCA2 and CDKN1A (p21) interacting protein. Previous studies have shown that down-regulation of BCCIP impairs recombinational DNA repair, G1/S cell cycle checkpoint, p53 trans-activation activity, cytokinesis, and chromosome stability, suggesting a potential role of BCCIP in cancer etiology. In this study, we investigated whether BCCIP is altered in astrocytomas. Methods Genomic DNA from 45 cases of grade IV astrocytic tumor (glioblastoma) tissues and 12 cases of normal tissues were analyzed by quantitative PCR. The BCCIP protein expression in 96 cases of grade II–IV astrocytic tumors was detected by immunohistochemistry (IHC). IHC staining of glial fibrillary acid protein (GFAP), a marker for astrocytic cells, was used to identify cells of the astrocytic lineage. Results We found that BCCIP protein is expressed in normal cells with positive staining of GFAP. However, BCCIP protein expression was not detectable in ~45% of all astrocytic tumors, and in > 60% in the grade IV glioblastoma. About 45% glioblastoma have significant (p < 0.01) reduction of BCCIP gene copy number when compared to normal DNA. Furthermore, the frequency of lacking BCCIP expression is associated with the aggressiveness of astrocytic tumors. Conclusion Our data implicate a role of BCCIP in astrocytic tumorigenesis, and lack of BCCIP may be used as a marker for astrocytomas.
Keywords	Neoplasms. Tumors. Oncology. Including cancer and carcinogens ; RC254-282 ; Internal medicine ; RC31-1245 ; Medicine ; R ; DOAJ:Oncology ; DOAJ:Medicine (General) ; DOAJ:Health Sciences
Subject code	570
Language	English
Publishing date	2009-08-01T00:00:00Z
Publisher	BioMed Central
Document type	Article ; Online
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Article ; Online: Filamin-A as a marker and target for DNA damage based cancer therapy.

Yue, Jingyin / Lu, Huimei / Liu, Jingmei / Berwick, Marianne / Shen, Zhiyuan

DNA repair

2011 Volume 11, Issue 2, Page(s) 192–200

Abstract: Filamin-A, also called actin binding protein 280 (ABP-280), cross-links the actin filaments into dynamic orthogonal network to serve as scaffolds in multiple signaling pathways. It has been reported that filamin-A interacts with DNA damage response ... ...

Abstract	Filamin-A, also called actin binding protein 280 (ABP-280), cross-links the actin filaments into dynamic orthogonal network to serve as scaffolds in multiple signaling pathways. It has been reported that filamin-A interacts with DNA damage response proteins BRCA1 and BRCA2. Defects of filamin-A impair the repair of DNA double strand breaks (DSBs), resulting in sensitization of cells to ionizing radiation. In this study, we sought to test the hypothesis that filamin-A can be used as a target for cancer chemotherapy and as a biomarker to predict cancer response to therapeutic DNA damage. We found that reduction of filamin-A sensitizes cancer cells to chemotherapy reagents bleomycin and cisplatin, delays the repair of not only DSBs but also single strand breaks (SSBs) and interstrand crosslinks (ICLs), and increases chromosome breaks after the drug treatment. By treating a panel of human melanoma cell lines with variable filamin-A expression, we observed a correlation between expression level of filamin-A protein and drug IC(50). We further inhibited the expression of filamin-A in melanoma cells, and found that this confers an increased sensitivity to bleomycin and cisplatin treatment in a mouse xenograft tumor model. These results suggest that filamin-A plays a role in repair of a variety of DNA damage, that lack of filamin-A is a prognostic marker for a better outcome after DNA damage based treatment, and filamin-A can be inhibited to sensitize filamin-A positive cancer cells to therapeutic DNA damage. Thus filamin-A can be used as a biomarker and a target for DNA damage based cancer therapy.
MeSH term(s)	Animals ; Antineoplastic Agents/pharmacology ; Antineoplastic Agents/therapeutic use ; Biomarkers, Tumor/deficiency ; Biomarkers, Tumor/metabolism ; Bleomycin/pharmacology ; Bleomycin/therapeutic use ; Cell Line, Tumor ; Chromosomal Instability/drug effects ; Cisplatin/pharmacology ; Cisplatin/therapeutic use ; Contractile Proteins/deficiency ; Contractile Proteins/metabolism ; DNA Breaks, Single-Stranded/drug effects ; DNA Damage ; DNA Repair/drug effects ; Filamins ; Gene Expression Regulation, Neoplastic/drug effects ; Humans ; Melanoma/drug therapy ; Melanoma/genetics ; Melanoma/metabolism ; Melanoma/pathology ; Mice ; Microfilament Proteins/deficiency ; Microfilament Proteins/metabolism ; Molecular Targeted Therapy/methods ; Prognosis ; Xenograft Model Antitumor Assays
Chemical Substances	Antineoplastic Agents ; Biomarkers, Tumor ; Contractile Proteins ; FLNC protein, human ; Filamins ; Microfilament Proteins ; Bleomycin (11056-06-7) ; Cisplatin (Q20Q21Q62J)
Language	English
Publishing date	2011-11-02
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2071608-4
ISSN	1568-7856 ; 1568-7864
ISSN (online)	1568-7856
ISSN	1568-7864
DOI	10.1016/j.dnarep.2011.10.019
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Inter-library loan at ZB MED

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Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito