LIVIVO - Search results -

Search results

Result 1 - 10 of total 12

Search options

Article ; Online: A binary module for microbiota-mediated regulation of γδ17 cells, hallmarked by microbiota-driven expression of programmed cell death protein 1.

Huang, Hsin-I / Xue, Yue / Jewell, Mark L / Tan, Chin Yee / Theriot, Barbara / Aggarwal, Nupur / Dockterman, Jacob / Lin, Yang-Ding / Schroeder, Erin A / Wang, Donghai / Xiong, Na / Coers, Jörn / Shinohara, Mari L / Surana, Neeraj K / Hammer, Gianna Elena

Cell reports

2023 Volume 42, Issue 9, Page(s) 113143

Language	English
Publishing date	2023-09-07
Publishing country	United States
Document type	Published Erratum
ZDB-ID	2649101-1
ISSN	2211-1247 ; 2211-1247
ISSN (online)	2211-1247
ISSN	2211-1247
DOI	10.1016/j.celrep.2023.113143
Database	MEDical Literature Analysis and Retrieval System OnLINE

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.

Article ; Online: A binary module for microbiota-mediated regulation of γδ17 cells, hallmarked by microbiota-driven expression of programmed cell death protein 1.

Cell reports

2023 Volume 42, Issue 8, Page(s) 112951

Abstract: Little is known about how microbiota regulate innate-like γδ T cells or how these restrict their effector functions within mucosal barriers, where microbiota provide chronic stimulation. Here, we show that microbiota-mediated regulation of γδ17 cells is ... ...

Abstract	Little is known about how microbiota regulate innate-like γδ T cells or how these restrict their effector functions within mucosal barriers, where microbiota provide chronic stimulation. Here, we show that microbiota-mediated regulation of γδ17 cells is binary, where microbiota instruct in situ interleukin-17 (IL-17) production and concomitant expression of the inhibitory receptor programmed cell death protein 1 (PD-1). Microbiota-driven expression of PD-1 and IL-17 and preferential adoption of a PD-1
MeSH term(s)	Humans ; Interleukin-17/metabolism ; Programmed Cell Death 1 Receptor ; Receptors, Antigen, T-Cell, gamma-delta/metabolism ; Inflammation/metabolism ; Microbiota
Chemical Substances	Interleukin-17 ; Programmed Cell Death 1 Receptor ; Receptors, Antigen, T-Cell, gamma-delta
Language	English
Publishing date	2023-08-08
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2649101-1
ISSN	2211-1247 ; 2211-1247
ISSN (online)	2211-1247
ISSN	2211-1247
DOI	10.1016/j.celrep.2023.112951
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article ; Online: A binary module for microbiota-mediated regulation of γδ17 cells, hallmarked by microbiota-driven expression of programmed cell death protein 1

Hsin-I Huang / Yue Xue / Mark L. Jewell / Chin Yee Tan / Barbara Theriot / Nupur Aggarwal / Jacob Dockterman / Yang-Ding Lin / Erin A. Schroeder / Donghai Wang / Na Xiong / Jörn Coers / Mari L. Shinohara / Neeraj K. Surana / Gianna Elena Hammer

Cell Reports, Vol 42, Iss 8, Pp 112951- (2023)

2023

Abstract: Summary: Little is known about how microbiota regulate innate-like γδ T cells or how these restrict their effector functions within mucosal barriers, where microbiota provide chronic stimulation. Here, we show that microbiota-mediated regulation of γδ17 ... ...

Abstract	Summary: Little is known about how microbiota regulate innate-like γδ T cells or how these restrict their effector functions within mucosal barriers, where microbiota provide chronic stimulation. Here, we show that microbiota-mediated regulation of γδ17 cells is binary, where microbiota instruct in situ interleukin-17 (IL-17) production and concomitant expression of the inhibitory receptor programmed cell death protein 1 (PD-1). Microbiota-driven expression of PD-1 and IL-17 and preferential adoption of a PD-1high phenotype are conserved for γδ17 cells across multiple mucosal barriers. Importantly, microbiota-driven PD-1 inhibits in situ IL-17 production by mucosa-resident γδ17 effectors, linking microbiota to their simultaneous activation and suppression. We further show the dynamic nature of this microbiota-driven module and define an inflammation-associated activation state for γδ17 cells marked by augmented PD-1, IL-17, and lipid uptake, thus linking the microbiota to dynamic subset-specific activation and metabolic remodeling to support γδ17 effector functions in a microbiota-dense tissue environment.
Keywords	CP: Immunology ; CP: Microbiology ; Biology (General) ; QH301-705.5
Language	English
Publishing date	2023-08-01T00:00:00Z
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.

Article ; Online: Molecular control of steady-state dendritic cell maturation and immune homeostasis.

Hammer, Gianna Elena / Ma, Averil

Annual review of immunology

2013 Volume 31, Page(s) 743–791

Abstract: Dendritic cells (DCs) are specialized sentinels responsible for coordinating adaptive immunity. This function is dependent upon coupled sensitivity to environmental signs of inflammation and infection to cellular maturation-the programmed alteration of ... ...

Abstract	Dendritic cells (DCs) are specialized sentinels responsible for coordinating adaptive immunity. This function is dependent upon coupled sensitivity to environmental signs of inflammation and infection to cellular maturation-the programmed alteration of DC phenotype and function to enhance immune cell activation. Although DCs are thus well equipped to respond to pathogens, maturation triggers are not unique to infection. Given that immune cells are exquisitely sensitive to the biological functions of DCs, we now appreciate that multiple layers of suppression are required to restrict the environmental sensitivity, cellular maturation, and even life span of DCs to prevent aberrant immune activation during the steady state. At the same time, steady-state DCs are not quiescent but rather perform key functions that support homeostasis of numerous cell types. Here we review these functions and molecular mechanisms of suppression that control steady-state DC maturation. Corruption of these steady-state operatives has diverse immunological consequences and pinpoints DCs as potent drivers of autoimmune and inflammatory disease.
MeSH term(s)	Animals ; Cell Differentiation/genetics ; Cell Differentiation/immunology ; Dendritic Cells/cytology ; Dendritic Cells/immunology ; Dendritic Cells/metabolism ; Homeostasis/genetics ; Homeostasis/immunology ; Humans ; Lectins, C-Type/physiology ; Membrane Glycoproteins/physiology ; Mice ; Receptors, Immunologic/physiology ; Receptors, Pattern Recognition/physiology ; Signal Transduction/genetics ; Signal Transduction/immunology ; Toll-Like Receptors/physiology
Chemical Substances	CLEC4A protein, human ; Dcir protein, mouse ; Lectins, C-Type ; Membrane Glycoproteins ; Receptors, Immunologic ; Receptors, Pattern Recognition ; Toll-Like Receptors
Language	English
Publishing date	2013-01-17
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	604953-9
ISSN	1545-3278 ; 0732-0582
ISSN (online)	1545-3278
ISSN	0732-0582
DOI	10.1146/annurev-immunol-020711-074929
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Se 849: 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 ; Online: A Requirement of Protein Geranylgeranylation for Chemokine Receptor Signaling and Th17 Cell Function in an Animal Model of Multiple Sclerosis.

Swan, Gregory / Geng, Jia / Park, Eunchong / Ding, Quanquan / Zhou, John / Walcott, Ciana / Zhang, Junyi J / Huang, Hsin-I / Hammer, Gianna Elena / Wang, Donghai

Frontiers in immunology

2021 Volume 12, Page(s) 641188

Abstract: Precisely controlled lymphocyte migration is critically required for immune surveillance and successful immune responses. Lymphocyte migration is strictly regulated by chemokines and chemokine receptors. Here we show that protein geranylgeranylation, a ... ...

Abstract	Precisely controlled lymphocyte migration is critically required for immune surveillance and successful immune responses. Lymphocyte migration is strictly regulated by chemokines and chemokine receptors. Here we show that protein geranylgeranylation, a form of post-translational protein lipid modification, is required for chemokine receptor-proximal signaling. Mature thymocytes deficient for protein geranylgeranylation are impaired for thymus egress. Circulating mature T cells lacking protein geranylgeranylation fail to home to secondary lymphoid organs or to transmigrate in response to chemokines
MeSH term(s)	Animals ; Cell Differentiation/immunology ; Chemotaxis, Leukocyte/immunology ; Encephalomyelitis, Autoimmune, Experimental/immunology ; Mice ; Multiple Sclerosis ; Protein Prenylation/immunology ; Receptors, Chemokine/immunology ; Signal Transduction/immunology ; Th17 Cells/immunology
Chemical Substances	Receptors, Chemokine
Language	English
Publishing date	2021-03-22
Publishing country	Switzerland
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2021.641188
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article ; Online: Th17 Immunity in the Colon Is Controlled by Two Novel Subsets of Colon-Specific Mononuclear Phagocytes.

Huang, Hsin-I / Jewell, Mark L / Youssef, Nourhan / Huang, Min-Nung / Hauser, Elizabeth R / Fee, Brian E / Rudemiller, Nathan P / Privratsky, Jamie R / Zhang, Junyi J / Reyes, Estefany Y / Wang, Donghai / Taylor, Gregory A / Gunn, Michael D / Ko, Dennis C / Cook, Donald N / Chandramohan, Vidyalakshmi / Crowley, Steven D / Hammer, Gianna Elena

Frontiers in immunology

2021 Volume 12, Page(s) 661290

Abstract: Intestinal immunity is coordinated by specialized mononuclear phagocyte populations, constituted by a diversity of cell subsets. Although the cell subsets constituting the mononuclear phagocyte network are thought to be similar in both small and large ... ...

Abstract	Intestinal immunity is coordinated by specialized mononuclear phagocyte populations, constituted by a diversity of cell subsets. Although the cell subsets constituting the mononuclear phagocyte network are thought to be similar in both small and large intestine, these organs have distinct anatomy, microbial composition, and immunological demands. Whether these distinctions demand organ-specific mononuclear phagocyte populations with dedicated organ-specific roles in immunity are unknown. Here we implement a new strategy to subset murine intestinal mononuclear phagocytes and identify two novel subsets which are colon-specific: a macrophage subset and a Th17-inducing dendritic cell (DC) subset. Colon-specific DCs and macrophages co-expressed CD24 and CD14, and surprisingly, both were dependent on the transcription factor IRF4. Novel IRF4-dependent CD14
MeSH term(s)	Animals ; Antigen-Presenting Cells/immunology ; Antigen-Presenting Cells/metabolism ; CD24 Antigen/immunology ; CD24 Antigen/metabolism ; Colon/cytology ; Colon/immunology ; Colon/metabolism ; Cytokines/genetics ; Cytokines/immunology ; Cytokines/metabolism ; Dendritic Cells/immunology ; Dendritic Cells/metabolism ; Gene Expression/immunology ; Interferon Regulatory Factors/immunology ; Interferon Regulatory Factors/metabolism ; Intestine, Small/immunology ; Lipopolysaccharide Receptors/immunology ; Lipopolysaccharide Receptors/metabolism ; Macrophages/immunology ; Macrophages/metabolism ; Mice, 129 Strain ; Mice, Knockout ; Mice, Transgenic ; Phagocytes/immunology ; Phagocytes/metabolism ; Receptor, Anaphylatoxin C5a/immunology ; Receptor, Anaphylatoxin C5a/metabolism ; Th17 Cells/immunology ; Th17 Cells/metabolism ; Mice
Chemical Substances	CD24 Antigen ; Cytokines ; Interferon Regulatory Factors ; Lipopolysaccharide Receptors ; Receptor, Anaphylatoxin C5a ; interferon regulatory factor-4
Language	English
Publishing date	2021-04-28
Publishing country	Switzerland
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2021.661290
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article ; Online: The Ubiquitin-Modifying Enzyme A20 Terminates C-Type Lectin Receptor Signals and Is a Suppressor of Host Defense against Systemic Fungal Infection.

Liang, Jie / Zhang, Junyi J / Huang, Hsin-I / Kanayama, Masashi / Youssef, Nourhan / Jin, Yingai J / Reyes, Estefany Y / Abram, Clare L / Yang, Shigao / Lowell, Clifford A / Wang, Donghai / Shao, Ling / Shinohara, Mari L / Zhang, Jennifer Y / Hammer, Gianna Elena

Infection and immunity

2020 Volume 88, Issue 9

Abstract: C-type lectin receptors (CLRs) play key roles in antifungal defense. CLR-induced NF-κB is central to CLR functions in immunity, and thus, molecules that control the amplitude of CLR-induced NF-κB could profoundly influence host defense against fungal ... ...

Abstract	C-type lectin receptors (CLRs) play key roles in antifungal defense. CLR-induced NF-κB is central to CLR functions in immunity, and thus, molecules that control the amplitude of CLR-induced NF-κB could profoundly influence host defense against fungal pathogens. However, little is known about the mechanisms that negatively regulate CLR-induced NF-κB, and molecules which act on the CLR family broadly and which directly regulate acute CLR-signaling cascades remain unidentified. Here, we identify the ubiquitin-editing enzyme A20 as a negative regulator of acute NF-κB activation downstream of multiple CLR pathways. Absence of A20 suppression results in exaggerated CLR responses in cells which are A20 deficient and also cells which are A20 haplosufficient, including multiple primary immune cells. Loss of a single allele of A20 results in enhanced defense against systemic
MeSH term(s)	Animals ; Bone Marrow Cells/immunology ; Bone Marrow Cells/microbiology ; Candida albicans/immunology ; Candida albicans/pathogenicity ; Candidiasis/genetics ; Candidiasis/immunology ; Candidiasis/microbiology ; Dendritic Cells/immunology ; Dendritic Cells/microbiology ; Female ; Fetus ; Host Microbial Interactions/genetics ; Host Microbial Interactions/immunology ; Immunity, Innate ; Lectins, C-Type/genetics ; Lectins, C-Type/immunology ; Liver/immunology ; Liver/microbiology ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Myeloid Differentiation Factor 88/genetics ; Myeloid Differentiation Factor 88/immunology ; NF-kappa B/genetics ; NF-kappa B/immunology ; Primary Cell Culture ; Protein Processing, Post-Translational ; Signal Transduction ; TNF Receptor-Associated Factor 6/genetics ; TNF Receptor-Associated Factor 6/immunology ; Tumor Necrosis Factor alpha-Induced Protein 3/deficiency ; Tumor Necrosis Factor alpha-Induced Protein 3/genetics ; Tumor Necrosis Factor alpha-Induced Protein 3/immunology ; Ubiquitin/genetics ; Ubiquitin/immunology ; Ubiquitination
Chemical Substances	Lectins, C-Type ; Myd88 protein, mouse ; Myeloid Differentiation Factor 88 ; NF-kappa B ; TNF Receptor-Associated Factor 6 ; TRAF6 protein, mouse ; Ubiquitin ; Tumor Necrosis Factor alpha-Induced Protein 3 (EC 3.4.19.12) ; Tnfaip3 protein, mouse (EC 3.4.22.-)
Language	English
Publishing date	2020-08-19
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	218698-6
ISSN	1098-5522 ; 0019-9567
ISSN (online)	1098-5522
ISSN	0019-9567
DOI	10.1128/IAI.00048-20
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 684: 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 ▾
- See ZB MED holdings
- Order with fees

Article: The final touches make perfect the peptide-MHC class I repertoire.

Hammer, Gianna Elena / Kanaseki, Takayuki / Shastri, Nilabh

Immunity

2007 Volume 26, Issue 4, Page(s) 397–406

Abstract: Major histocompatibility complex (MHC) class I molecules present short, perfectly cleaved peptides on the cell surface for immune surveillance by CD8(+) T cells. The pathway for generating these peptides begins in the cytoplasm, and the peptide-MHC I ( ... ...

Abstract	Major histocompatibility complex (MHC) class I molecules present short, perfectly cleaved peptides on the cell surface for immune surveillance by CD8(+) T cells. The pathway for generating these peptides begins in the cytoplasm, and the peptide-MHC I (pMHC I) repertoire is finalized in the endoplasmic reticulum. Recent studies show that the peptides for MHC I are customized by the ER aminopeptidase associated with antigen processing and by dynamic interactions within the MHC peptide-loading complex. Failure to customize the pMHC I repertoire has profound immunological consequences.
MeSH term(s)	Animals ; Cytoplasm/immunology ; Endoplasmic Reticulum/enzymology ; Endoplasmic Reticulum/immunology ; Histocompatibility Antigens Class I/metabolism ; Humans ; Leucyl Aminopeptidase/deficiency ; Leucyl Aminopeptidase/genetics ; Leucyl Aminopeptidase/metabolism ; Membrane Transport Proteins/metabolism ; Oxidation-Reduction ; Peptides/immunology ; Peptides/metabolism ; Protein Disulfide-Isomerases/metabolism
Chemical Substances	Histocompatibility Antigens Class I ; Membrane Transport Proteins ; Peptides ; tapasin ; Leucyl Aminopeptidase (EC 3.4.11.1) ; puromycin-insensitive leucyl-specific aminopeptidase (EC 3.4.11.1) ; Protein Disulfide-Isomerases (EC 5.3.4.1)
Language	English
Publishing date	2007-04
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	1217235-2
ISSN	1097-4180 ; 1074-7613
ISSN (online)	1097-4180
ISSN	1074-7613
DOI	10.1016/j.immuni.2007.04.003
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 4227: 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)
Zs.MG 69: Show issues

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article: In the absence of aminopeptidase ERAAP, MHC class I molecules present many unstable and highly immunogenic peptides.

Hammer, Gianna Elena / Gonzalez, Federico / James, Edward / Nolla, Hector / Shastri, Nilabh

Nature immunology

2007 Volume 8, Issue 1, Page(s) 101–108

Abstract: Immunosurveillance by cytotoxic T cells requires that cells generate a diverse spectrum of peptides for presentation by major histocompatibility complex (MHC) class I molecules. Those peptides are generated by proteolysis, which begins in the cytoplasm ... ...

Abstract	Immunosurveillance by cytotoxic T cells requires that cells generate a diverse spectrum of peptides for presentation by major histocompatibility complex (MHC) class I molecules. Those peptides are generated by proteolysis, which begins in the cytoplasm and continues in the endoplasmic reticulum by the unique aminopeptidase ERAAP. The overall extent to which trimming by ERAAP modifies the peptide pool and the immunological consequences of ERAAP deficiency are unknown. Here we show that the peptide-MHC repertoire of ERAAP-deficient mice was missing many peptides. Furthermore, ERAAP-deficient cells presented many unstable and structurally unique peptide-MHC complexes, which elicited potent CD8+ T cell and B cell responses. Thus, ERAAP is a 'quintessential editor' of the peptide-MHC repertoire and, paradoxically, its absence enhances immunogenicity.
MeSH term(s)	Animals ; Antigen Presentation/immunology ; CD8-Positive T-Lymphocytes/immunology ; Cells, Cultured ; Female ; Histocompatibility Antigens Class I/immunology ; Leucyl Aminopeptidase/deficiency ; Leucyl Aminopeptidase/genetics ; Ligands ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Peptides/immunology
Chemical Substances	Histocompatibility Antigens Class I ; Ligands ; Peptides ; Leucyl Aminopeptidase (EC 3.4.11.1) ; puromycin-insensitive leucyl-specific aminopeptidase (EC 3.4.11.1)
Language	English
Publishing date	2007-01
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2016987-5
ISSN	1529-2916 ; 1529-2908
ISSN (online)	1529-2916
ISSN	1529-2908
DOI	10.1038/ni1409
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 5294: 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)
Zs.MG 42: Show issues

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article: ERAAP synergizes with MHC class I molecules to make the final cut in the antigenic peptide precursors in the endoplasmic reticulum.

Kanaseki, Takayuki / Blanchard, Nicolas / Hammer, Gianna Elena / Gonzalez, Federico / Shastri, Nilabh

Immunity

2006 Volume 25, Issue 5, Page(s) 795–806

Abstract: The major histocompatibility complex class I molecules display peptides (pMHC I) on the cell surface for immune surveillance by CD8(+) T cells. These peptides are generated by proteolysis of intracellular polypeptides by the proteasome in the cytoplasm ... ...

Abstract	The major histocompatibility complex class I molecules display peptides (pMHC I) on the cell surface for immune surveillance by CD8(+) T cells. These peptides are generated by proteolysis of intracellular polypeptides by the proteasome in the cytoplasm and then in the endoplasmic reticulum (ER) by the ER aminopeptidase associated with antigen processing (ERAAP). To define the unknown mechanism of ERAAP function in vivo, we analyzed naturally processed peptides in cells with or without appropriate MHC I and ERAAP. In the absence of MHC I, ERAAP degraded the antigenic precursors in the ER. However, MHC I molecules could bind proteolytic intermediates and were essential for generation of the final peptide by ERAAP. Thus, ERAAP synergizes with MHC I to generate the final pMHC I repertoire.
MeSH term(s)	Amino Acid Sequence ; Animals ; Antigen Presentation/physiology ; Antigens/chemistry ; Antigens/immunology ; Chromatography, High Pressure Liquid ; Endoplasmic Reticulum/immunology ; Endoplasmic Reticulum/metabolism ; HeLa Cells ; Histocompatibility Antigens Class I/immunology ; Histocompatibility Antigens Class I/metabolism ; Humans ; Immunoblotting ; Immunohistochemistry ; Leucyl Aminopeptidase/genetics ; Leucyl Aminopeptidase/immunology ; Leucyl Aminopeptidase/metabolism ; Lymphocyte Activation/immunology ; Mice ; Molecular Sequence Data ; Peptides/chemistry ; Peptides/immunology ; Polymerase Chain Reaction ; Transfection
Chemical Substances	Antigens ; Histocompatibility Antigens Class I ; Peptides ; Leucyl Aminopeptidase (EC 3.4.11.1) ; puromycin-insensitive leucyl-specific aminopeptidase (EC 3.4.11.1)
Language	English
Publishing date	2006-11
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1217235-2
ISSN	1097-4180 ; 1074-7613
ISSN (online)	1097-4180
ISSN	1074-7613
DOI	10.1016/j.immuni.2006.09.012
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Full text

In stock of ZB MED Cologne/Königswinter

Zs.A 4227: 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)
Zs.MG 69: Show issues

Order via subito

Details ▾

To top

More links

Kategorien

Order via subito

More links

Kategorien

Order via subito

Full text online

More links

Kategorien

Inter-library loan at ZB MED

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

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