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Article ; Online: Enhancing medical student diversity through a premedical program: A Caribbean school case study.

DeCarvalho, Helena / Lindner, Inna / Sengupta, Anamika / Rajput, Vijay / Raskin, Gannady

Education for health (Abingdon, England)

2018 Volume 31, Issue 1, Page(s) 48–51

Abstract: Background: Physicians with backgrounds underrepresented in medicine (URiM) are more likely to practice in underserved communities. Recruitment into and assistance during medical education has the potential to increase the number of URiM physicians. ... ...

Abstract	Background: Physicians with backgrounds underrepresented in medicine (URiM) are more likely to practice in underserved communities. Recruitment into and assistance during medical education has the potential to increase the number of URiM physicians. This study analyzes URiM students' academic performance at a well-established Caribbean school with and without prior successful completion of the Medical Education Readiness Program (MERP). Methods: A retrospective analysis of premedical school requirements and achievements in medical school were performed for URiM students enrolled in Ross University School of Medicine between 2006 and 2012, through either MERP or direct admission. For MERP and non-MERP students, an independent sample two-tailed Student t-test was used to compare prerequisite Grade Point Average (p GPA), Medical College Admission Test (MCAT), and The United States Medical Licensing Examination (USMLE) Step 1 scores. Chi-square analysis was performed to compare the attrition rates for MERP and non-MERP URiM students in the first years of medical schools well as USMLE Step 1 pass rates. Results: A total of 1299 students entering medical school directly (n = 981) or through MERP (n = 318) were evaluated. The mean MCAT (19.6 for MERP vs. 21.6 for non-MERP, P < 0.001) and prerequisite GPA (2.8 for MERP vs. 3.1 for non-MERP, P < 0.001) were significantly lower for the MERP students. A similar percentage of MERP and non-MERP students reached the 2 Discussion: MERP-like programs can help URiM students with lower undergraduate scores succeed in medical school.
MeSH term(s)	African Americans/education ; Caribbean Region ; Education, Medical/methods ; Hispanic Americans/education ; Humans ; Indians, North American/education ; Minority Groups/education ; Retrospective Studies ; Students, Medical ; United States
Language	English
Publishing date	2018-08-17
Publishing country	India
Document type	Journal Article
ZDB-ID	1318454-4
ISSN	1469-5804 ; 1357-6283
ISSN (online)	1469-5804
ISSN	1357-6283
DOI	10.4103/1357-6283.239047
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Article ; Online: 6,7-dihydroxy-3,4-dihydroisoquinoline: a novel inhibitor of nuclear factor-kappaB and in vitro invasion in murine mammary cancer cells.

Alvarez, Francisco N / Carlson, Louise M / Lindner, Inna / Lee, Kelvin P

Chemotherapy

2009 Volume 55, Issue 3, Page(s) 175–182

Abstract: Background: The inhibition of nuclear factor (NF)-kappaB with nontoxic agents is a promising possible treatment approach that may inhibit tumor cell proliferation, counteract the prosurvival pathways that mediate resistance to cytotoxic therapy, and ... ...

Abstract	Background: The inhibition of nuclear factor (NF)-kappaB with nontoxic agents is a promising possible treatment approach that may inhibit tumor cell proliferation, counteract the prosurvival pathways that mediate resistance to cytotoxic therapy, and prevent tumor cell metastasis. Methods: An initial structure-activity relationship study of the NF-kappaB inhibitory activity of acetophenone-type compounds using electrophoretic mobility shift assay and Western blot analysis is presented. An in vitro cell invasion assay using DA3 cells, a murine breast cancer cell line, was conducted to model antimetastatic activity. Results: The carbonyl moiety is found to be the functional group responsible for inhibition of NF-kappaB, and a novel, more effective agent, 6,7-dihydroxy-3,4-dihydroisoquinoline, is postulated and confirmed. The compounds are characterized as active in the inhibition of both the canonical and noncanonical NF-kappaB signaling pathways. Lastly, 6,7-dihydroxy-3,4-dihydroisoquinoline is discovered to inhibit in vitro invasion in DA3 cells. Conclusion: 6,7-Dihydroxy-3,4-dihydroisoquionoline and its derivatives are presented as potential prototypes for a novel series of nontoxic antimetastatic agents that can be used in conjunction with current cancer therapeutic techniques.
MeSH term(s)	Acetophenones/pharmacology ; Animals ; Antineoplastic Agents/pharmacology ; Isoquinolines/chemistry ; Isoquinolines/pharmacology ; Mammary Neoplasms, Animal/metabolism ; Mammary Neoplasms, Animal/pathology ; Mice ; NF-kappa B/antagonists & inhibitors ; NF-kappa B/metabolism ; Neoplasm Invasiveness ; Signal Transduction ; Structure-Activity Relationship ; Tumor Cells, Cultured
Chemical Substances	6,7-dihydroxy-3,4-dihydroisoquinoline ; Acetophenones ; Antineoplastic Agents ; Isoquinolines ; NF-kappa B
Language	English
Publishing date	2009
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	6708-8
ISSN	1421-9794 ; 0009-3157
ISSN (online)	1421-9794
ISSN	0009-3157
DOI	10.1159/000215303
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Article ; Online: Tumor-induced STAT3 signaling in myeloid cells impairs dendritic cell generation by decreasing PKCβII abundance.

Farren, Matthew R / Carlson, Louise M / Netherby, Colleen S / Lindner, Inna / Li, Pui-Kai / Gabrilovich, Dmitry I / Abrams, Scott I / Lee, Kelvin P

Science signaling

2014 Volume 7, Issue 313, Page(s) ra16

Abstract: A major mechanism by which cancers escape control by the immune system is by blocking the differentiation of myeloid cells into dendritic cells (DCs), immunostimulatory cells that activate antitumor T cells. Tumor-dependent activation of signal ... ...

Abstract	A major mechanism by which cancers escape control by the immune system is by blocking the differentiation of myeloid cells into dendritic cells (DCs), immunostimulatory cells that activate antitumor T cells. Tumor-dependent activation of signal transducer and activator of transcription 3 (STAT3) signaling in myeloid progenitor cells is thought to cause this block in their differentiation. In addition, a signaling pathway through protein kinase C βII (PKCβII) is essential for the differentiation of myeloid cells into DCs. We found in humans and mice that breast cancer cells substantially decreased the abundance of PKCβII in myeloid progenitor cells through a mechanism involving the enhanced activation of STAT3 signaling by soluble, tumor-derived factors (TDFs). STAT3 bound to previously undescribed negative regulatory elements within the promoter of PRKCB, which encodes PKCβII. We also found a previously undescribed counter-regulatory mechanism through which the activity of PKCβII inhibited tumor-dependent STAT3 signaling by decreasing the abundance of cell surface receptors, such as cytokine and growth factor receptors, that are activated by TDFs. Together, these data suggest that a previously unrecognized cross-talk mechanism between the STAT3 and PKCβII signaling pathways provides the molecular basis for the tumor-induced blockade in the differentiation of myeloid cells, and suggest that enhancing PKCβII activity may be a therapeutic strategy to alleviate cancer-mediated suppression of the immune system.
MeSH term(s)	Animals ; Breast Neoplasms/genetics ; Breast Neoplasms/immunology ; Breast Neoplasms/metabolism ; Breast Neoplasms/pathology ; Breast Neoplasms/therapy ; Dendritic Cells/immunology ; Dendritic Cells/metabolism ; Dendritic Cells/pathology ; Female ; Humans ; K562 Cells ; Mammary Neoplasms, Animal/genetics ; Mammary Neoplasms, Animal/immunology ; Mammary Neoplasms, Animal/pathology ; Mammary Neoplasms, Animal/therapy ; Mice ; Mice, Inbred BALB C ; Myeloid Progenitor Cells ; Neoplasm Proteins/genetics ; Neoplasm Proteins/immunology ; Protein Kinase C beta/genetics ; Protein Kinase C beta/immunology ; Protein Kinase C beta/metabolism ; Response Elements/immunology ; STAT3 Transcription Factor/genetics ; STAT3 Transcription Factor/immunology ; STAT3 Transcription Factor/metabolism ; Signal Transduction/genetics ; Signal Transduction/immunology
Chemical Substances	Neoplasm Proteins ; STAT3 Transcription Factor ; STAT3 protein, human ; Stat3 protein, mouse ; PRKCB protein, human (EC 2.7.11.13) ; Protein Kinase C beta (EC 2.7.11.13)
Language	English
Publishing date	2014-02-18
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2417226-1
ISSN	1937-9145 ; 1945-0877
ISSN (online)	1937-9145
ISSN	1945-0877
DOI	10.1126/scisignal.2004656
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Article ; Online: A pre-matriculation learning program that enables medical students with low prerequisite scores to succeed.

Lindner, Inna / Sacks, David / Sheakley, Maria / Seidel, Charles / Wahlig, Bruce C / Rojas, Jose D / Coleman, Mary T

Medical teacher

2013 Volume 35, Issue 10, Page(s) 872–873

MeSH term(s)	Achievement ; Education, Medical, Undergraduate/organization & administration ; Educational Measurement ; Humans ; Learning ; Students, Medical
Language	English
Publishing date	2013-10
Publishing country	England
Document type	Letter
ZDB-ID	424426-6
ISSN	1466-187X ; 0142-159X
ISSN (online)	1466-187X
ISSN	0142-159X
DOI	10.3109/0142159X.2013.786812
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Article: 6,7-Dihydroxy-3,4-Dihydroisoquinoline: A Novel Inhibitor of Nuclear Factor-κB and in vitro Invasion in Murine Mammary Cancer Cells

Alvarez, Francisco N. / Carlson, Louise M. / Lindner, Inna / Lee, Kelvin P.

Chemotherapy

2009 Volume 55, Issue 3, Page(s) 175–182

Abstract: Background: The inhibition of nuclear factor (NF)-κB with nontoxic agents is a promising possible treatment approach that may inhibit tumor cell proliferation, counteract the prosurvival pathways that mediate resistance to cytotoxic therapy, and prevent ... ...

Institution	Pine Crest School, Ft. Lauderdale, Fla., and Department of Microbiology and Immunology, University of Miami Leonard M. Miller School of Medicine, Miami, Fla., USA
Abstract	Background: The inhibition of nuclear factor (NF)-κB with nontoxic agents is a promising possible treatment approach that may inhibit tumor cell proliferation, counteract the prosurvival pathways that mediate resistance to cytotoxic therapy, and prevent tumor cell metastasis. Methods: An initial structure-activity relationship study of the NF-κB inhibitory activity of acetophenone-type compounds using electrophoretic mobility shift assay and Western blot analysis is presented. An in vitro cell invasion assay using DA3 cells, a murine breast cancer cell line, was conducted to model antimetastatic activity. Results: The carbonyl moiety is found to be the functional group responsible for inhibition of NF-κB, and a novel, more effective agent, 6,7-dihydroxy-3,4-dihydroisoquinoline, is postulated and confirmed. The compounds are characterized as active in the inhibition of both the canonical and noncanonical NF-κB signaling pathways. Lastly, 6,7-dihydroxy-3,4-dihydroisoquinoline is discovered to inhibit in vitro invasion in DA3 cells. Conclusion: 6,7-Dihydroxy-3,4-dihydroisoquionoline and its derivatives are presented as potential prototypes for a novel series of nontoxic antimetastatic agents that can be used in conjunction with current cancer therapeutic techniques.
Keywords	Quantitative structure-activity relationship analysis ; Acetophenones ; Nuclear factor-ĸB ; Metastasis
Language	English
Publishing date	2009-04-30
Publisher	S. Karger AG
Publishing place	Basel, Switzerland
Document type	Article
Note	Pharmacology
ZDB-ID	6708-8
ISSN	1421-9794 ; 0009-3157
ISSN (online)	1421-9794
ISSN	0009-3157
DOI	10.1159/000215303
Database	Karger publisher's database

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Article: Signal transduction in DC differentiation: winged messengers and Achilles' heel.

Lindner, Inna / Cejas, Pedro J / Carlson, Louise M / Torruellas, Julie / Plano, Gregory V / Lee, Kelvin P

Advances in experimental medicine and biology

2007 Volume 590, Page(s) 1–29

MeSH term(s)	Animals ; Bacterial Proteins/physiology ; Cell Differentiation/drug effects ; Cell Differentiation/physiology ; Cell Lineage ; Cytokines/pharmacology ; Cytokines/physiology ; Dendritic Cells/classification ; Dendritic Cells/cytology ; Dendritic Cells/immunology ; Dendritic Cells/metabolism ; Hematopoietic Stem Cells/cytology ; Hematopoietic Stem Cells/drug effects ; Humans ; Intracellular Signaling Peptides and Proteins/pharmacology ; Intracellular Signaling Peptides and Proteins/physiology ; Lymphocytes/cytology ; Lymphocytes/drug effects ; Mice ; Mitogen-Activated Protein Kinases/physiology ; Models, Immunological ; Myeloid Cells/cytology ; Myeloid Cells/drug effects ; NF-kappa B/physiology ; Neoplastic Stem Cells/cytology ; Neoplastic Stem Cells/drug effects ; Protein Kinase C/physiology ; Signal Transduction/physiology ; Transcription Factor RelB/physiology ; Yersinia Infections/immunology ; Yersinia pestis/physiology
Chemical Substances	Bacterial Proteins ; Cytokines ; Intracellular Signaling Peptides and Proteins ; NF-kappa B ; RELB protein, human ; Relb protein, mouse ; YopP protein, Yersinia ; Transcription Factor RelB (147337-75-5) ; Protein Kinase C (EC 2.7.11.13) ; Mitogen-Activated Protein Kinases (EC 2.7.11.24)
Language	English
Publishing date	2007
Publishing country	United States
Document type	Journal Article ; Review
ISSN	2214-8019 ; 0065-2598
ISSN (online)	2214-8019
ISSN	0065-2598
DOI	10.1007/978-0-387-34814-8_1
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Article: Protein kinase C blockade inhibits differentiation of myeloid blasts into dendritic cells by calcium ionophore A23187.

Li, Qian / Ozer, Howard / Lindner, Inna / Lee, Kelvin P / Kharfan-Dabaja, Mohamed A

International journal of hematology

2005 Volume 81, Issue 2, Page(s) 131–137

Abstract: Direct differentiation of myeloid leukemia blasts into antigen-presenting dendritic cells (DCs) for use as cellular vaccines is unique in that identification of tumor-specific antigens may not be necessary because the antigens should already be ... ...

Abstract	Direct differentiation of myeloid leukemia blasts into antigen-presenting dendritic cells (DCs) for use as cellular vaccines is unique in that identification of tumor-specific antigens may not be necessary because the antigens should already be endogenously expressed. We hypothesized that signaling through protein kinase C (PKC) is required for differentiation of HL-60 promyeloblasts into DCs upon stimulation with calcium ionophore A23187. To demonstrate the inhibitory effect of PKC blockade, we pretreated HL-60 myeloid blasts with the protein kinase inhibitor bisindolylmaleimide I (Bis-1) for 24 hours and then treated the cells with calcium ionophore A23187 for an additional 24 hours. Controls consisted of HL-60 blasts treated with A23187, Bis-1 alone, or media. We noted that blasts cultured in media, Bis-1, or Bis-1 then A23187 did not develop the morphologic and phenotypic DC characteristics, up-regulate Rel B, or activate allogeneic T-cells. Our findings suggested that PKC blockade inhibits morphologic, phenotypic, and functional differentiation of HL-60 promyeloblasts into antigen-presenting DCs. Our findings supported the role of PKC as an obligatory pathway for calcium ionophore A23187-induced differentiation of HL-60 myeloblasts into antigen-presenting DCs.
MeSH term(s)	Antigen-Presenting Cells ; Calcimycin/pharmacology ; Cell Differentiation/drug effects ; Dendritic Cells/cytology ; Dendritic Cells/immunology ; HL-60 Cells ; Humans ; Immunotherapy, Adoptive/methods ; Indoles/pharmacology ; Leukemia, Myeloid, Acute ; Leukemia, Promyelocytic, Acute/pathology ; Maleimides/pharmacology ; Protein Kinase C/antagonists & inhibitors ; Protein Kinase C/physiology ; Proto-Oncogene Proteins/genetics ; T-Lymphocytes/immunology ; Transcription Factor RelB ; Transcription Factors/genetics ; Up-Regulation/drug effects
Chemical Substances	Indoles ; Maleimides ; Proto-Oncogene Proteins ; RELB protein, human ; Transcription Factors ; Transcription Factor RelB (147337-75-5) ; Calcimycin (37H9VM9WZL) ; Protein Kinase C (EC 2.7.11.13) ; bisindolylmaleimide I (L79H6N0V6C)
Language	English
Publishing date	2005-02-23
Publishing country	Japan
Document type	Journal Article
ZDB-ID	1076875-0
ISSN	1865-3774 ; 0925-5710 ; 0917-1258
ISSN (online)	1865-3774
ISSN	0925-5710 ; 0917-1258
DOI	10.1532/ijh97.na0405
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Article: Modulation of dendritic cell differentiation and function by YopJ of Yersinia pestis.

Lindner, Inna / Torruellas-Garcia, Julie / Torrvellas-Garcia, Julie / Kolonias, Despina / Carlson, Louise M / Tolba, Khaled A / Plano, Gregory V / Lee, Kelvin P

European journal of immunology

2007 Volume 37, Issue 9, Page(s) 2450–2462

Abstract: Yersinia pestis evades immune responses in part by injecting into host immune cells several effector proteins called Yersinia outer proteins (Yops) that impair cellular function. This has been best characterized in the innate effector cells, but much ... ...

Abstract	Yersinia pestis evades immune responses in part by injecting into host immune cells several effector proteins called Yersinia outer proteins (Yops) that impair cellular function. This has been best characterized in the innate effector cells, but much less so for cells involved in adaptive immune responses. Dendritic cells (DC) sit at the crossroads between innate and adaptive immunity, and can function to initiate or inhibit adaptive immune responses. Although Y. pestis can target and inactivate DC, the mechanism responsible for this remains unclear. We have found that injection of Y. pestis YopJ into DC progenitors disrupts key signal transduction pathways and interferes with DC differentiation and subsequent function. YopJ injection prevents up-regulation of the NF-kappaB transcription factor Rel B and inhibits MAPK/ERK activation--both having key roles in DC differentiation. Furthermore, YopJ injection prevents costimulatory ligand up-regulation, LPS-induced cytokine expression, and yields differentiated DC with diminished capability to induce T cell proliferation and IFN-gamma induction. By modulating DC function through YopJ-mediated disruption of signaling pathways during progenitor to DC differentiation, Yersinia may interfere with the adaptive responses necessary to clear the infection as well as establish a tolerant immune environment that leads to chronic infection/carrier state in the surviving host.
MeSH term(s)	Bacterial Proteins/genetics ; Bacterial Proteins/immunology ; Bacterial Proteins/metabolism ; Cell Differentiation/immunology ; Cell Survival ; Cells, Cultured ; Cytokines/biosynthesis ; Dendritic Cells/cytology ; Dendritic Cells/drug effects ; Dendritic Cells/immunology ; Humans ; Ligands ; Lipopolysaccharides/pharmacology ; Recombinant Proteins/genetics ; Recombinant Proteins/immunology ; Recombinant Proteins/metabolism ; T-Lymphocytes/cytology ; T-Lymphocytes/immunology ; Yersinia pestis/classification ; Yersinia pestis/immunology
Chemical Substances	Bacterial Proteins ; Cytokines ; Ligands ; Lipopolysaccharides ; Recombinant Proteins ; YopP protein, Yersinia
Language	English
Publishing date	2007-09
Publishing country	Germany
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	120108-6
ISSN	1521-4141 ; 0014-2980
ISSN (online)	1521-4141
ISSN	0014-2980
DOI	10.1002/eji.200635947
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Article: Modulation of dendritic cell differentiation and function by YopJ of Yersinia pestis

Lindner, Inna / Torrvellas-Garcia, Julie / Kolonias, Despina / Carlson, Louise M / Tolba, Khaled A / Plano, Gregory V / Lee, Kelvin P

European journal of immunology. 2007 Sept., v. 37, no. 9

2007

Abstract	Yersinia pestis evades immune responses in part by injecting into host immune cells several effector proteins called Yersinia outer proteins (Yops) that impair cellular function. This has been best characterized in the innate effector cells, but much less so for cells involved in adaptive immune responses. Dendritic cells (DC) sit at the crossroads between innate and adaptive immunity, and can function to initiate or inhibit adaptive immune responses. Although Y. pestis can target and inactivate DC, the mechanism responsible for this remains unclear. We have found that injection of Y. pestis YopJ into DC progenitors disrupts key signal transduction pathways and interferes with DC differentiation and subsequent function. YopJ injection prevents up-regulation of the NF-κB transcription factor Rel B and inhibits MAPK/ERK activation - both having key roles in DC differentiation. Furthermore, YopJ injection prevents costimulatory ligand up-regulation, LPS-induced cytokine expression, and yields differentiated DC with diminished capability to induce T cell proliferation and IFN-γ induction. By modulating DC function through YopJ-mediated disruption of signaling pathways during progenitor to DC differentiation, Yersinia may interfere with the adaptive responses necessary to clear the infection as well as establish a tolerant immune environment that leads to chronic infection/carrier state in the surviving host.
Language	English
Dates of publication	2007-09
Size	p. 2450-2462.
Publishing place	Wiley-VCH Verlag
Document type	Article
ZDB-ID	120108-6
ISSN	1521-4141 ; 0014-2980
ISSN (online)	1521-4141
ISSN	0014-2980
DOI	10.1002/eji.200635947
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Article: Regulation of RelB expression during the initiation of dendritic cell differentiation.

Cejas, Pedro J / Carlson, Louise M / Kolonias, Despina / Zhang, Jian / Lindner, Inna / Billadeau, Daniel D / Boise, Lawrence H / Lee, Kelvin P

Molecular and cellular biology

2005 Volume 25, Issue 17, Page(s) 7900–7916

Abstract: The transcription factor RelB is required for proper development and function of dendritic cells (DCs), and its expression is upregulated early during differentiation from a variety of progenitors. We explored this mechanism of upregulation in the KG1 ... ...

Abstract	The transcription factor RelB is required for proper development and function of dendritic cells (DCs), and its expression is upregulated early during differentiation from a variety of progenitors. We explored this mechanism of upregulation in the KG1 cell line model of a DC progenitor and in the differentiation-resistant KG1a subline. RelB expression is relatively higher in untreated KG1a cells but is upregulated only during differentiation of KG1 by an early enhancement of transcriptional elongation, followed by an increase in transcription initiation. Restoration of protein kinase CbetaII (PKCbetaII) expression in KG1a cells allows them to differentiate into DCs. We show that PKCbetaII also downregulated constitutive expression of NF-kappaB in KG1a-transfected cells and restores the upregulation of RelB during differentiation by increased transcriptional initiation and elongation. The two mechanisms are independent and sensitive to PKC signaling levels. Conversely, RelB upregulation was inhibited in primary human monocytes where PKCbetaII expression was knocked down by small interfering RNA targeting. Altogether, the data show that RelB expression during DC differentiation is controlled by PKCbetaII-mediated regulation of transcriptional initiation and elongation.
MeSH term(s)	Cell Differentiation ; Cells, Cultured ; Dendritic Cells/cytology ; Dendritic Cells/metabolism ; Gene Expression Regulation/drug effects ; Gene Expression Regulation/genetics ; Humans ; Promoter Regions, Genetic/genetics ; Protein Kinase C/genetics ; Protein Kinase C/metabolism ; Protein Kinase C beta ; Proto-Oncogene Proteins/genetics ; Proto-Oncogene Proteins/metabolism ; RNA Stability ; RNA, Small Interfering/genetics ; Tetradecanoylphorbol Acetate/pharmacology ; Transcription Factor RelB ; Transcription Factors/genetics ; Transcription Factors/metabolism ; Transcription, Genetic/drug effects ; Transcription, Genetic/genetics
Chemical Substances	Proto-Oncogene Proteins ; RELB protein, human ; RNA, Small Interfering ; Transcription Factors ; Transcription Factor RelB (147337-75-5) ; Protein Kinase C (EC 2.7.11.13) ; Protein Kinase C beta (EC 2.7.11.13) ; Tetradecanoylphorbol Acetate (NI40JAQ945)
Language	English
Publishing date	2005-09
Publishing country	United States
Document type	Journal Article
ZDB-ID	779397-2
ISSN	1098-5549 ; 0270-7306
ISSN (online)	1098-5549
ISSN	0270-7306
DOI	10.1128/MCB.25.17.7900-7916.2005
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