LIVIVO - Search results -

Search results

Result 1 - 10 of total 26

Search options

Article ; Online: Adenoviral virotherapy for malignant brain tumors.

Nandi, Suvobroto / Lesniak, Maciej S

2009 Volume 9, Issue 6, Page(s) 737–747

Abstract: Glioblastoma multiforme is the most common form of primary brain cancer. In the past decade, virotherapy of tumors has gained credence, particularly in glioma management, as these tumors are not completely resectable and tend to micro-metastasize. ... ...

Abstract	Glioblastoma multiforme is the most common form of primary brain cancer. In the past decade, virotherapy of tumors has gained credence, particularly in glioma management, as these tumors are not completely resectable and tend to micro-metastasize. Adenoviral vectors have an advantage over other viral vectors in that they are relatively non-toxic and do not integrate in the genome. However, the lack of coxsackie and adenovirus receptors on surface of gliomas provides for inefficient transduction of wild-type adenoviral vectors in these tumors. By targeting receptors that are overexpressed in gliomas, modified adenoviral constructs have been shown to efficiently infect glioma cells. In addition, by taking advantage of tumor-specific promoter elements, oncolytic adenoviral vectors offer the promise of selective tumor-specific replication. This dual targeting strategy has enabled specificity in both laboratory and pre-clinical settings. This review examines current trends in adenoviral virotherapy of gliomas, with an emphasis on targeting modalities and future clinical applications.
MeSH term(s)	Adenoviridae/physiology ; Apoptosis ; Brain Neoplasms/pathology ; Brain Neoplasms/therapy ; Glioblastoma/pathology ; Glioblastoma/therapy ; Humans ; Oncolytic Virotherapy ; Virus Replication
Language	English
Publishing date	2009-05-20
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2052501-1
ISSN	1744-7682 ; 1471-2598
ISSN (online)	1744-7682
ISSN	1471-2598
DOI	10.1517/14712590902988451
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

In stock of ZB MED Cologne/Königswinter

Zs.A 6094: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
ab Jg. 2022: Lesesaal (EG)

Order via subito

This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

Details ▾

Article: The oncogene mcts1.

Hachem, Ali / Nandi, Suvobroto

Translational oncogenomics

2007 Volume 2, Page(s) 79–84

Abstract: The oncogene MCTS1, discovered as an amplified product in a subset of T-cell lymphoma lines, has been implicated in cell cycle progression and conferring a growth advantage in lymphomas and breast cancer. Recent research shows that it modulates the MAPK ... ...

Abstract	The oncogene MCTS1, discovered as an amplified product in a subset of T-cell lymphoma lines, has been implicated in cell cycle progression and conferring a growth advantage in lymphomas and breast cancer. Recent research shows that it modulates the MAPK pathway and acts as a translational activator both in vivo and in vitro. In breast cancer cells, expression of MCTS1 confers aggressive properties and inhibits apoptosis. This article will review these data and its implications on our understanding of cancer.
Language	English
Publishing date	2007-07-19
Publishing country	United States
Document type	Journal Article
ZDB-ID	2424421-1
ISSN	1177-2727
ISSN	1177-2727
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article ; Online: The role of chemokine receptor CXCR4 in lung cancer.

Gangadhar, Tara / Nandi, Suvobroto / Salgia, Ravi

Cancer biology & therapy

2010 Volume 9, Issue 6, Page(s) 409–416

Abstract: Lung cancer is the leading cause of cancer deaths worldwide. Small cell lung cancer (SCLC), which comprises 15% of all lung cancers, is almost exclusively due to smoking and is highly aggressive due to early widespread metastasis. While combination ... ...

Abstract	Lung cancer is the leading cause of cancer deaths worldwide. Small cell lung cancer (SCLC), which comprises 15% of all lung cancers, is almost exclusively due to smoking and is highly aggressive due to early widespread metastasis. While combination chemotherapy has lead to modest improvements in outcome, the five-year overall survival for SCLC remains at 5%. Identifying distinct biochemical pathways of metastasis and chemotherapy resistance in SCLC may lead to novel therapeutic approaches and improve survival in SCLC patients. The chemokine receptor CXCR4 is emerging as an important target in cancer growth, metastasis, relapse and resistance to therapy. In this article, we review the structure and function of CXCR4 and its ligand, CXCL12, as well as mechanisms of CXCR4/CXCL12 signal transduction in lung cancer. We review the current preclinical and translational research involving this pathway in lung cancer and the clinical development of several novel agents targeting the CXCR4/CXCL12 pathway. Further understanding of the CXCR4/CXCL12 pathway in SCLC and NSCLC may provide a rationale for innovative research on the CXCR4 receptor as a potential novel therapeutic target in lung cancer.
MeSH term(s)	Antineoplastic Agents/pharmacology ; Antineoplastic Agents/therapeutic use ; Carcinoma, Bronchogenic/drug therapy ; Carcinoma, Non-Small-Cell Lung/drug therapy ; Carcinoma, Non-Small-Cell Lung/metabolism ; Carcinoma, Non-Small-Cell Lung/pathology ; Chemokine CXCL12 ; Chemokines/pharmacology ; Chemokines/therapeutic use ; Humans ; Lung Neoplasms/drug therapy ; Lung Neoplasms/metabolism ; Lung Neoplasms/pathology ; Receptors, CXCR4/genetics ; Receptors, CXCR4/metabolism ; Receptors, CXCR4/physiology ; Receptors, Chemokine/therapeutic use ; Signal Transduction/drug effects ; Signal Transduction/physiology ; Small Cell Lung Carcinoma ; Translational Medical Research
Chemical Substances	Antineoplastic Agents ; Chemokine CXCL12 ; Chemokines ; Receptors, CXCR4 ; Receptors, Chemokine
Language	English
Publishing date	2010-03-18
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2146305-0
ISSN	1555-8576 ; 1538-4047
ISSN (online)	1555-8576
ISSN	1538-4047
DOI	10.4161/cbt.9.6.11233
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 5887: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (2.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Inhibition of Sonic hedgehog and Notch pathways enhances sensitivity of CD133(+) glioma stem cells to temozolomide therapy.

Ulasov, Ilya V / Nandi, Suvobroto / Dey, Mahua / Sonabend, Adam M / Lesniak, Maciej S

Molecular medicine (Cambridge, Mass.)

2010 Volume 17, Issue 1-2, Page(s) 103–112

Abstract: Malignant gliomas are currently treated with temozolomide (TMZ), but often exhibit resistance to this agent. CD133(+) cancer stem cells, a population believed to contribute to the tumor's chemoresistance, bear the activation of Notch and Sonic hedgehog ( ... ...

Abstract	Malignant gliomas are currently treated with temozolomide (TMZ), but often exhibit resistance to this agent. CD133(+) cancer stem cells, a population believed to contribute to the tumor's chemoresistance, bear the activation of Notch and Sonic hedgehog (SHH) pathways. In this study, we examined whether inhibition of both pathways enhances the efficacy of TMZ monotherapy in the context of glioma stem cells. Transcriptional analysis of Notch and SHH pathways in CD133(+)-enriched glioma cell populations showed the activity of these pathways. CD133(+) cells were less susceptible to TMZ treatment than the unsorted glioma counterparts. Interestingly, Notch and SHH pathway transcriptional activity in CD133(+) glioma cells was further enhanced by TMZ exposure, which led to NOTCH 1, NCOR2, and GLI1 upregulation (6.64-, 3.73-, and 2.79-fold, respectively) and CFLAR downregulation (4.22-fold). The therapeutic effect of TMZ was enhanced by Notch and SHH pathway pharmacological antagonism with GSI-1 and cyclopamine. More importantly, simultaneous treatment involving TMZ with both of these compounds led to a significant increase in CD133(+) glioma cytotoxicity than treatment with any of these agents alone (P < 0.05). In conclusion, CD133(+) glioma cells overexpress genes involved in Notch and SHH pathways. These pathways contribute to the chemoresistant phenotype of CD133(+) glioma cells, as their antagonism leads to an additive effect when used in combination with TMZ.
MeSH term(s)	AC133 Antigen ; Antigens, CD ; Antigens, Surface ; Antineoplastic Agents, Alkylating/pharmacology ; Brain Neoplasms/drug therapy ; Brain Neoplasms/genetics ; Cell Line, Tumor ; Dacarbazine/analogs & derivatives ; Dacarbazine/pharmacology ; Drug Resistance, Neoplasm/drug effects ; Drug Resistance, Neoplasm/genetics ; Gene Expression Profiling ; Gene Expression Regulation, Neoplastic ; Glioma/drug therapy ; Glioma/genetics ; Glycoproteins ; Hedgehog Proteins/antagonists & inhibitors ; Hedgehog Proteins/metabolism ; Humans ; Neoplastic Stem Cells/drug effects ; Neoplastic Stem Cells/metabolism ; Peptides ; Receptors, Notch/antagonists & inhibitors ; Receptors, Notch/metabolism ; Signal Transduction ; Temozolomide ; Tumor Cells, Cultured
Chemical Substances	AC133 Antigen ; Antigens, CD ; Antigens, Surface ; Antineoplastic Agents, Alkylating ; Glycoproteins ; Hedgehog Proteins ; PROM1 protein, human ; Peptides ; Receptors, Notch ; Dacarbazine (7GR28W0FJI) ; Temozolomide (YF1K15M17Y)
Language	English
Publishing date	2010-10-15
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1283676-x
ISSN	1528-3658 ; 1076-1551
ISSN (online)	1528-3658
ISSN	1076-1551
DOI	10.2119/molmed.2010.00062
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 4456: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (2.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Short hairpin RNA-mediated fibronectin knockdown delays tumor growth in a mouse glioma model.

Sengupta, Sadhak / Nandi, Suvobroto / Hindi, Enal S / Wainwright, Derek A / Han, Yu / Lesniak, Maciej S

Neoplasia (New York, N.Y.)

2010 Volume 12, Issue 10, Page(s) 837–847

Abstract: Glioblastoma multiforme is the most common and lethal primary brain tumor. Glioma progression depends on the rapid proliferation of tumor cells accompanied by an acute immunosuppressive environment, facilitated mainly by tumor infiltration of regulatory ... ...

Abstract	Glioblastoma multiforme is the most common and lethal primary brain tumor. Glioma progression depends on the rapid proliferation of tumor cells accompanied by an acute immunosuppressive environment, facilitated mainly by tumor infiltration of regulatory T cells (Tregs). In this study, we characterize the role of fibronectin, a high-molecular weight extracellular matrix glycoprotein secreted by tumor cells, in controlling glioma progression and in mediating immunosuppression. Fibronectin binds to membrane-spanning integrin receptors and plays an important role in cell signaling, in defining cellular shape, in mobility, and in regulating the cell cycle. We found that inhibition of fibronectin expression in glioma cells, using short hairpin RNA-mediated silencing of gene expression, delayed cell proliferation in vitro. This delayed growth is explained, in part, by the observed reduced expression of integrin β(1) fibronectin receptor, which was restored by the inhibition of proteosomal activity. In our analysis of the downstream signaling targets of integrin β(1), we demonstrated reduced phosphorylation of Src kinase and STAT-3. We also observed reduced survivin expression that induced a three-fold increased accumulation of fibronectin-knockdown cells in the G(2)/M phase. In an experimental animal model, the fibronectin knockdown tumors had a mean survival advantage of 23 days over wild-type tumors. Moreover, brain samples of animals bearing fibronectin-knockdown tumors showed delayed Treg recruitment. Collectively, we propose that fibronectin is a key mediator of glioma progression because its inhibition delays both tumor progression and immunosuppression.
MeSH term(s)	Animals ; Apoptosis/drug effects ; Blotting, Western ; Brain Neoplasms/genetics ; Brain Neoplasms/metabolism ; Brain Neoplasms/therapy ; Cell Division/physiology ; Cell Proliferation ; Cysteine Proteinase Inhibitors/pharmacology ; Disease Models, Animal ; Fibronectins/genetics ; Fibronectins/metabolism ; Flow Cytometry ; G2 Phase/physiology ; Glioma/genetics ; Glioma/metabolism ; Glioma/therapy ; Humans ; Immunoenzyme Techniques ; Inhibitor of Apoptosis Proteins/genetics ; Inhibitor of Apoptosis Proteins/metabolism ; Integrin beta1/genetics ; Integrin beta1/metabolism ; Leupeptins/pharmacology ; Male ; Mice ; Mice, Inbred C57BL ; Phosphorylation/drug effects ; RNA, Messenger/genetics ; RNA, Small Interfering/genetics ; Repressor Proteins/genetics ; Repressor Proteins/metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; STAT3 Transcription Factor/genetics ; STAT3 Transcription Factor/metabolism ; Signal Transduction/drug effects ; Survivin ; T-Lymphocytes, Regulatory ; Tumor Cells, Cultured ; src-Family Kinases/genetics ; src-Family Kinases/metabolism
Chemical Substances	Birc5 protein, mouse ; Cysteine Proteinase Inhibitors ; Fibronectins ; Inhibitor of Apoptosis Proteins ; Integrin beta1 ; Leupeptins ; RNA, Messenger ; RNA, Small Interfering ; Repressor Proteins ; STAT3 Transcription Factor ; Stat3 protein, mouse ; Survivin ; src-Family Kinases (EC 2.7.10.2) ; benzyloxycarbonylleucyl-leucyl-leucine aldehyde (RF1P63GW3K)
Language	English
Publishing date	2010-08-20
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1483840-0
ISSN	1476-5586 ; 1522-8002
ISSN (online)	1476-5586
ISSN	1522-8002
DOI	10.1593/neo.10662
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 5203: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (2.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: A chimeric adenovirus with an Ad 3 fiber knob modification augments glioma virotherapy.

Nandi, Suvobroto / Ulasov, Ilya V / Rolle, Cleo E / Han, Yu / Lesniak, Maciej S

The journal of gene medicine

2009 Volume 11, Issue 11, Page(s) 1005–1011

Abstract: Background: Malignant gliomas remain refractory to treatment despite advances in chemotherapy and surgical techniques. Viral vectors developed to treat gliomas have had low transduction capabilities, limiting their use. Gliomas over-express CD46, CD80, ... ...

Abstract	Background: Malignant gliomas remain refractory to treatment despite advances in chemotherapy and surgical techniques. Viral vectors developed to treat gliomas have had low transduction capabilities, limiting their use. Gliomas over-express CD46, CD80, and CD86, all of which bind adenovirus serotype 3. Methods: To increase the infectivity and replication of oncolytic vectors in malignant brain tumors, we created a conditionally replicating adenovirus, CRAd-Survivin-5/3, which contains a survivin promoter-driving E1A and a chimeric fiber consisting of adenovirus serotype 3 knob. Results: In vitro, this modified CRAd showed ten- to 100-fold increased cytotoxicity against glioma cells. Ex vivo analysis of primary glioblastoma multiforme samples infected with CRAd-Survivin-5/3 showed an increase in cytotoxicity of 20-30% compared to adenovirus wild-type (AdWT). In normal human astrocytes and normal brain tissues, CRAd-Survivin-5/3 exhibited 30-40% and 10-15% lower cytotoxicity than AdWT, respectively. In an intracranial xenograft model of glioma, this oncolytic virus increased tumor-free survival and overall lifespan by 50% compared to controls (p < 0.05). Conclusions: CRAd-Survivin-5/3 represents an attractive alternative to existing vectors and should be tested further in the pre-clinical setting.
MeSH term(s)	Adenoviridae/genetics ; Adenoviridae/metabolism ; Brain Neoplasms/metabolism ; Brain Neoplasms/therapy ; Cell Line, Tumor ; Genetic Vectors/genetics ; Glioma/metabolism ; Glioma/therapy ; Humans ; Microtubule-Associated Proteins/genetics ; Microtubule-Associated Proteins/metabolism ; Oncolytic Virotherapy/methods
Chemical Substances	Microtubule-Associated Proteins
Language	English
Publishing date	2009-08-18
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1458024-x
ISSN	1521-2254 ; 1099-498X
ISSN (online)	1521-2254
ISSN	1099-498X
DOI	10.1002/jgm.1385
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

In stock of ZB MED Cologne/Königswinter

Zs.A 5423: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (2.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾

Article: Characterization of the MCT-1 pseudogene: identification and implication of its location in a highly amplified region of chromosome 20.

Nandi, Suvobroto / Shi, Bo / Perreault, Jonathan / Gartenhaus, Ronald B

Biochimica et biophysica acta

2006 Volume 1759, Issue 5, Page(s) 234–239

Abstract: The MCT-1 oncogene was initially identified as an amplified gene on chromosome Xq22-24 in a T-cell lymphoma. MCT-1 is over-expressed in a subset of diffuse large B-cell lymphoma (DLBCL), a common form of Non-Hodgkin's Lymphoma (NHL). We have identified a ...

Abstract	The MCT-1 oncogene was initially identified as an amplified gene on chromosome Xq22-24 in a T-cell lymphoma. MCT-1 is over-expressed in a subset of diffuse large B-cell lymphoma (DLBCL), a common form of Non-Hodgkin's Lymphoma (NHL). We have identified a pseudogene for MCT-1 (PsiMCT-1) that is located on chromosome 20q11.2, a region within an amplicon containing several important genes frequently amplified in certain breast and ovarian cancers. Genomic analysis revealed that PsiMCT-1 is a processed pseudogene. Interestingly, both MCT-1 and its pseudogene are located on regions of the genome that are frequently amplified in several different human malignancies. MCT-1 is the oldest known oncogene and its insertion as a pseudogene occurred at a later time point in evolution. Existence of PsiMCT-1 should be considered when analyzing genomic amplification and or expression of MCT-1. Analysis of MCT-1 and PsiMCT-1 might provide clues to cancer genes and their evolution across species.
MeSH term(s)	Amino Acid Sequence ; Breast Neoplasms/genetics ; Cell Cycle Proteins/genetics ; Chromosomes, Human, Pair 20/genetics ; DNA/analysis ; Evolution, Molecular ; Female ; Gene Amplification ; Humans ; In Situ Hybridization, Fluorescence ; Molecular Sequence Data ; Oncogene Proteins/genetics ; Ovarian Neoplasms/genetics ; Physical Chromosome Mapping ; Pseudogenes/genetics
Chemical Substances	Cell Cycle Proteins ; MCTS1 protein, human ; Oncogene Proteins ; DNA (9007-49-2)
Language	English
Publishing date	2006-05
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	60-7
ISSN	1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650 ; 0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
ISSN (online)	1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650
ISSN	0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
DOI	10.1016/j.bbaexp.2006.05.003
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Uc I Zs.247: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article: Mutation in the relA gene of Vibrio cholerae affects in vitro and in vivo expression of virulence factors.

Haralalka, Shruti / Nandi, Suvobroto / Bhadra, Rupak K

Journal of bacteriology

2003 Volume 185, Issue 16, Page(s) 4672–4682

Abstract: The relA gene product determines the level of (p)ppGpp, the effector nucleotides of the bacterial stringent response that are also involved in the regulation of other functions, like antibiotic production and quorum sensing. In order to explore the ... ...

Abstract	The relA gene product determines the level of (p)ppGpp, the effector nucleotides of the bacterial stringent response that are also involved in the regulation of other functions, like antibiotic production and quorum sensing. In order to explore the possible involvement of relA in the regulation of virulence of Vibrio cholerae, a relA homolog from the organism (relA(VCH)) was cloned and sequenced. The relA(VCH) gene encodes a 738-amino-acid protein having functions similar to those of other gram-negative bacteria, including Escherichia coli. A deltarelA::kan allele was generated by replacing approximately 31% of the open reading frame of wild-type relA of V. cholerae El Tor strain C6709 with a kanamycin resistance gene. The V. cholerae relA mutant strain thus generated, SHK17, failed to accumulate (p)ppGpp upon amino acid deprivation. Interestingly, compared to the wild type, C6709, the mutant strain SHK17 exhibited significantly reduced in vitro production of two principal virulence factors, cholera toxin (CT) and toxin-coregulated pilus (TCP), under virulence gene-inducing conditions. In vivo experiments carried out in rabbit ileal loop and suckling mouse models also confirmed our in vitro results. The data suggest that (p)ppGpp is essential for maximal expression of CT and TCP during in vitro growth, as well as during intestinal infection by virulent V. cholerae. Northern blot and reverse transcriptase PCR analyses indicated significant reduction in the transcript levels of both virulence factors in the relA mutant strain SHK17. Such marked alteration of virulence phenotypes in SHK17 appears most likely to be due to down regulation of transcript levels of toxR and toxT, the two most important virulence regulatory genes of V. cholerae. In SHK17, the altered expression of the two outer membrane porin proteins, OmpU and OmpT, indicated that the relA mutation most likely affects the ToxR-dependent virulence regulatory pathway, because it had been shown earlier that ToxR directly regulates their expression independently of ToxT.
MeSH term(s)	Animals ; Bacterial Proteins/biosynthesis ; Bacterial Proteins/genetics ; Cholera/virology ; Cholera Toxin/biosynthesis ; Cholera Toxin/genetics ; Gene Expression Regulation, Bacterial ; Guanosine Pentaphosphate/metabolism ; Ileum/microbiology ; Intestines/microbiology ; Ligases/genetics ; Ligases/metabolism ; Mice ; Molecular Sequence Data ; Mutation ; Rabbits ; Sequence Analysis, DNA ; Vibrio cholerae/genetics ; Vibrio cholerae/pathogenicity ; Virulence/genetics ; Virulence Factors/genetics ; Virulence Factors/metabolism
Chemical Substances	Bacterial Proteins ; Virulence Factors ; Guanosine Pentaphosphate (38918-96-6) ; Cholera Toxin (9012-63-9) ; Ligases (EC 6.-) ; guanosine 3',5'-polyphosphate synthetases (EC 6.-)
Language	English
Publishing date	2003-07-31
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2968-3
ISSN	1098-5530 ; 0021-9193
ISSN (online)	1098-5530
ISSN	0021-9193
DOI	10.1128/JB.185.16.4672-4682.2003
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Ud II Zs.50: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article: Integration of metal-resistant determinants from the plasmid of an Acidocella strain into the chromosome of Escherichia coli DH5alpha.

Ghosh, Sajalendu / Mahapatra, Nitish R / Nandi, Suvobroto / Banerjee, Pataki C

Current microbiology

2005 Volume 50, Issue 1, Page(s) 28–32

Abstract: Acidophilic bacteria of mine origin are ideal systems for studying microbial metal resistance because of their ability to grow in the presence of high concentrations of metal salts. We have previously shown that the metal-resistant transformants obtained ...

Abstract	Acidophilic bacteria of mine origin are ideal systems for studying microbial metal resistance because of their ability to grow in the presence of high concentrations of metal salts. We have previously shown that the metal-resistant transformants obtained after transformation of Escherichia coli DH5alpha with plasmid DNA preparation from Acidocella sp. strain GS19h did not contain any plasmid suggesting chromosomal integration of the plasmid(s) (Appl Environ Microbiol 1997; 63: 4523-4527). The present study provides evidence in support of this suggestion. The pulsed field gel electrophoresis (PFGE) pattern of genomic DNA of the plasmidless metal-resistant transformants differed markedly from that of the untransformed DH5alpha strain. Moreover, when the recombinant plasmids constructed by cloning plasmid DNA fragments of the Acidocella strain GS19h in the vector pBluescript II KS+ were used to transform E. coli DH5alpha strain, no plasmid DNA was detected in some of the zinc- and ampicillin-resistant (ZnrAmpr) clones. The PFGE pattern of genomic DNA of such a transformed clone also differed markedly from that of the parent strain, suggesting chromosomal integration of the recombinant plasmid(s) containing both ampicillin- and zinc-resistance determinants. This observation was further supported by hybridization of chromosomal DNA of the plasmidless ZnrAmpr E. coli DH5alpha clone with the probes made from the plasmid DNA of strain GS19h and the vector DNA. Thus, this study corroborates our previous finding and documents the phenomenon of integration of metal-resistant determinants from the Acidocella GS19h plasmid(s) into the chromosome of E. coli DH5alpha.
MeSH term(s)	Bacteria/drug effects ; Bacteria/genetics ; Chromosomes, Bacterial ; Drug Resistance, Microbial ; Electrophoresis, Gel, Pulsed-Field ; Escherichia coli/genetics ; Metals/pharmacology ; Plasmids
Chemical Substances	Metals
Language	English
Publishing date	2005-01
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	134238-1
ISSN	1432-0991 ; 0343-8651
ISSN (online)	1432-0991
ISSN	0343-8651
DOI	10.1007/s00284-004-4370-z
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

In stock of ZB MED Cologne/Königswinter

Zs.A 1446: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (1.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾

Article ; Online: Short Hairpin RNA-Mediated Fibronectin Knockdown Delays Tumor Growth in a Mouse Glioma Model

Sadhak Sengupta / Suvobroto Nandi / Enal S. Hindi / Derek A. Wainwright / Yu Han / Maciej S. Lesniak

Neoplasia : An International Journal for Oncology Research, Vol 12, Iss 10, Pp 837-

2010 Volume 847

Abstract	Glioblastoma multiforme is the most common and lethal primary brain tumor. Glioma progression depends on the rapid proliferation of tumor cells accompanied by an acute immunosuppressive environment, facilitated mainly by tumor infiltration of regulatory T cells (Tregs). In this study, we characterize the role of fibronectin, a high-molecular weight extracellular matrix glycoprotein secreted by tumor cells, in controlling glioma progression and in mediating immunosuppression. Fibronectin binds to membrane-spanning integrin receptors and plays an important role in cell signaling, in defining cellular shape, in mobility, and in regulating the cell cycle. We found that inhibition of fibronectin expression in glioma cells, using short hairpin RNA-mediated silencing of gene expression, delayed cell proliferation in vitro. This delayed growth is explained, in part, by the observed reduced expression of integrin β1 fibronectin receptor, which was restored by the inhibition of proteosomal activity. In our analysis of the downstream signaling targets of integrin β1, we demonstrated reduced phosphorylation of Src kinase and STAT-3. We also observed reduced survivin expression that induced a three-fold increased accumulation of fibronectin-knockdown cells in the G2/M phase. In an experimental animal model, the fibronectin knockdown tumors had a mean survival advantage of 23 days over wild-type tumors. Moreover, brain samples of animals bearing fibronectin-knockdown tumors showed delayed Treg recruitment. Collectively, we propose that fibronectin is a key mediator of glioma progression because its inhibition delays both tumor progression and immunosuppression.
Keywords	Medicine ; R ; Internal medicine ; RC31-1245 ; Neoplasms. Tumors. Oncology. Including cancer and carcinogens ; RC254-282
Publishing date	2010-10-01T00:00:00Z
Publisher	Elsevier
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

Full text online

Full text

Inter-library loan at ZB MED

Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

To top

Full text online

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

Full text online

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

Full text online

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

Full text online

More links

Kategorien

Inter-library loan at ZB MED