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Article: Cbl and Cbl-b Ubiquitin Ligases are Essential for Intestinal Epithelial Stem Cell Maintenance.

Zutshi, Neha / Mohapatra, Bhopal C / Mondal, Pinaki / An, Wei / Goetz, Benjamin T / Wang, Shuo / Li, Sicong / Storck, Matthew D / Mercer, David F / Black, Adrian R / Thayer, Sarah P / Black, Jennifer D / Lin, Chi / Band, Vimla / Band, Hamid

bioRxiv : the preprint server for biology

2023

Abstract: Among the signaling pathways that control the stem cell self-renewal and maintenance vs. acquisition of differentiated cell fates, those mediated by receptor tyrosine kinase (RTK) activation are well established as key players. CBL family ubiquitin ... ...

Abstract	Among the signaling pathways that control the stem cell self-renewal and maintenance vs. acquisition of differentiated cell fates, those mediated by receptor tyrosine kinase (RTK) activation are well established as key players. CBL family ubiquitin ligases are negative regulators of RTKs but their physiological roles in regulating stem cell behaviors are unclear. While hematopoietic
Language	English
Publishing date	2023-05-22
Publishing country	United States
Document type	Preprint
DOI	10.1101/2023.05.17.541154
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Article ; Online: The histone deacetylase inhibitor M344 as a multifaceted therapy for pancreatic cancer.

Knoche, Shelby M / Brumfield, Gabrielle L / Goetz, Benjamin T / Sliker, Bailee H / Larson, Alaina C / Olson, Madeline T / Poelaert, Brittany J / Bavari, Audrey / Yan, Ying / Black, Jennifer D / Solheim, Joyce C

PloS one

2022 Volume 17, Issue 9, Page(s) e0273518

Abstract: The histone deacetylase (HDAC) inhibitor vorinostat, used with gemcitabine and other therapies, has been effective in treatment of experimental models of pancreatic cancer. In this study, we demonstrated that M344, an HDAC inhibitor, is efficacious ... ...

Abstract	The histone deacetylase (HDAC) inhibitor vorinostat, used with gemcitabine and other therapies, has been effective in treatment of experimental models of pancreatic cancer. In this study, we demonstrated that M344, an HDAC inhibitor, is efficacious against pancreatic cancer in vitro and in vivo, alone or with gemcitabine. By 24 hours post-treatment, M344 augments the population of pancreatic cancer cells in G1, and at a later time point (48 hours) it increases apoptosis. M344 inhibits histone H3 deacetylation and slows pancreatic cancer cell proliferation better than vorinostat, and it does not decrease the viability of a non-malignant cell line more than vorinostat. M344 also elevates pancreatic cancer cell major histocompatibility complex (MHC) class I molecule expression, potentially increasing the susceptibility of pancreatic cancer cells to T cell lysis. Taken together, our findings support further investigation of M344 as a pancreatic cancer treatment.
MeSH term(s)	Cell Line, Tumor ; Histone Deacetylase Inhibitors/pharmacology ; Histone Deacetylase Inhibitors/therapeutic use ; Histone Deacetylases/metabolism ; Histones/metabolism ; Humans ; Hydroxamic Acids/pharmacology ; Hydroxamic Acids/therapeutic use ; Pancreatic Neoplasms/drug therapy ; Vorinostat/pharmacology
Chemical Substances	Histone Deacetylase Inhibitors ; Histones ; Hydroxamic Acids ; Vorinostat (58IFB293JI) ; Histone Deacetylases (EC 3.5.1.98)
Language	English
Publishing date	2022-09-20
Publishing country	United States
Document type	Journal Article
ZDB-ID	2267670-3
ISSN	1932-6203 ; 1932-6203
ISSN (online)	1932-6203
ISSN	1932-6203
DOI	10.1371/journal.pone.0273518
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Article ; Online: HLA-B influences integrin beta-1 expression and pancreatic cancer cell migration.

Sliker, Bailee H / Goetz, Benjamin T / Barnes, Raina / King, Hannah / Maurer, H Carlo / Olive, Kenneth P / Solheim, Joyce C

Experimental cell research

2020 Volume 390, Issue 2, Page(s) 111960

Abstract: Human leukocyte antigen (HLA) class I molecules present antigenic peptides to cytotoxic T cells, causing lysis of malignant cells. Transplantation biology studies have implicated HLA class I molecules in cell migration, but there has been little evidence ...

Abstract	Human leukocyte antigen (HLA) class I molecules present antigenic peptides to cytotoxic T cells, causing lysis of malignant cells. Transplantation biology studies have implicated HLA class I molecules in cell migration, but there has been little evidence presented that they influence cancer cell migration, a contributing factor in metastasis. In this study, we examined the effect of HLA-B on pancreatic cancer cell migration. HLA-B siRNA transfection increased the migration of the S2-013 pancreatic cancer cells but, in contrast, reduced migration of the PANC-1 and MIA PaCa-2 pancreatic cancer cell lines. Integrin molecules have previously been implicated in the upregulation of pancreatic cancer cell migration, and knockdown of HLA-B in S2-013 cells heightened the expression of integrin beta 1 (ITGB1), but in the PANC-1 and MIA PaCa-2 cells HLA-B knockdown diminished ITGB1 expression. A transmembrane sequence in an S2-013 HLA-B heavy chain matches a corresponding sequence in HLA-B in the BxPC-3 pancreatic cancer cell line, and knockdown of BxPC-3 HLA-B mimics the effect of S2-013 HLA-B knockdown on migration. In total, our findings indicate that HLA-B influences the expression of ITGB1 in pancreatic cancer cells, with concurrent distinctions in transmembrane sequences and effects on the migration of the cells.
MeSH term(s)	Cell Line, Tumor ; Cell Movement/genetics ; Cell Proliferation ; Focal Adhesion Kinase 1/genetics ; Focal Adhesion Kinase 1/metabolism ; Gene Expression Regulation, Neoplastic ; HLA-B Antigens/genetics ; HLA-B Antigens/metabolism ; Humans ; Integrin alpha2/genetics ; Integrin alpha2/metabolism ; Integrin beta1/genetics ; Integrin beta1/metabolism ; Organ Specificity ; Pancreas/metabolism ; Pancreas/pathology ; Protein Isoforms/antagonists & inhibitors ; Protein Isoforms/genetics ; Protein Isoforms/metabolism ; RNA, Small Interfering/genetics ; RNA, Small Interfering/metabolism ; Signal Transduction
Chemical Substances	HLA-B Antigens ; ITGA2B protein, human ; Integrin alpha2 ; Integrin beta1 ; Itgb1 protein, human ; Protein Isoforms ; RNA, Small Interfering ; Focal Adhesion Kinase 1 (EC 2.7.10.2) ; PTK2 protein, human (EC 2.7.10.2)
Language	English
Publishing date	2020-03-16
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1493-x
ISSN	1090-2422 ; 0014-4827
ISSN (online)	1090-2422
ISSN	0014-4827
DOI	10.1016/j.yexcr.2020.111960
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Article ; Online: Beta 2-microglobulin regulates amyloid precursor-like protein 2 expression and the migration of pancreatic cancer cells.

Sliker, Bailee H / Goetz, Benjamin T / Peters, Haley L / Poelaert, Brittany J / Borgstahl, Gloria E O / Solheim, Joyce C

Cancer biology & therapy

2019 Volume 20, Issue 6, Page(s) 931–940

Abstract: Beta 2-microglobulin ( ... ...

Abstract	Beta 2-microglobulin (β
MeSH term(s)	Amyloid beta-Protein Precursor/genetics ; Cell Line, Tumor ; Cell Movement/genetics ; Gene Expression Regulation, Neoplastic ; Gene Knockdown Techniques ; Histocompatibility Antigens Class I/genetics ; Humans ; Nerve Tissue Proteins/genetics ; Pancreatic Neoplasms/genetics ; beta 2-Microglobulin/genetics ; beta 2-Microglobulin/metabolism
Chemical Substances	APLP2 protein, human ; Amyloid beta-Protein Precursor ; Histocompatibility Antigens Class I ; Nerve Tissue Proteins ; beta 2-Microglobulin
Language	English
Publishing date	2019-02-27
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2146305-0
ISSN	1555-8576 ; 1538-4047
ISSN (online)	1555-8576
ISSN	1538-4047
DOI	10.1080/15384047.2019.1580414
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Article ; Online: Nanoformulation of CCL21 greatly increases its effectiveness as an immunotherapy for neuroblastoma.

Poelaert, Brittany J / Romanova, Svetlana / Knoche, Shelby M / Olson, Madeline T / Sliker, Bailee H / Smits, Kaitlin / Dickey, Brittney L / Moffitt-Holida, Alexandra E J / Goetz, Benjamin T / Khan, Nuzhat / Smith, Lynette / Band, Hamid / Mohs, Aaron M / Coulter, Donald W / Bronich, Tatiana K / Solheim, Joyce C

Journal of controlled release : official journal of the Controlled Release Society

2020 Volume 327, Page(s) 266–283

Abstract: Neuroblastoma is the most commonly diagnosed extracranial solid tumor in children. The patients with aggressive metastatic disease or refractory/relapsed neuroblastoma currently face a dismally low chance of survival. Thus, there is a great need for more ...

Abstract	Neuroblastoma is the most commonly diagnosed extracranial solid tumor in children. The patients with aggressive metastatic disease or refractory/relapsed neuroblastoma currently face a dismally low chance of survival. Thus, there is a great need for more effective therapies for this illness. In previous studies, we, as well as others, showed that the immune cell chemoattractant C-C motif chemokine ligand 21 (CCL21) is effective as an intratumoral therapy able to slow the growth of cancers. In this current study, we developed and tested an injectable, slow-release, uniform, and optimally loaded alginate nanoformulation of CCL21 as a means to provide prolonged intratumoral treatment. The alginate-nanoformulated CCL21, when injected intratumorally into mice bearing neuroblastoma lesions, significantly prolonged survival and decreased the tumor growth rate compared to CCL21 alone, empty nanoparticles, or buffer. Notably, we also observed complete tumor clearance and subsequent full protection against tumor rechallenge in 33% of nanoformulated CCL21-treated mice. Greater intratumoral presence of nanoformulated CCL21, compared to free CCL21, at days 1 and 2 after treatment ended was confirmed through fluorescent labeling and tracking. Nanoformulated CCL21-treated tumors exhibited a general pattern of prolonged increases in anti-tumor cytokines and relatively lower levels of pro-tumor cytokines in comparison to tumors treated with CCL21 alone or buffer only. Thus, this novel nanoformulation of CCL21 is an effective treatment for neuroblastoma, and may have potential for the delivery of CCL21 to other types of solid tumors in the future and as a slow-release delivery modality for other immunotherapies.
MeSH term(s)	Animals ; Cell Line, Tumor ; Chemokine CCL21/therapeutic use ; Humans ; Immunotherapy ; Ligands ; Mice ; Neuroblastoma/drug therapy
Chemical Substances	CCL21 protein, human ; Chemokine CCL21 ; Ligands
Language	English
Publishing date	2020-07-22
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	632533-6
ISSN	1873-4995 ; 0168-3659
ISSN (online)	1873-4995
ISSN	0168-3659
DOI	10.1016/j.jconrel.2020.07.024
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Article: Nanoformulation of CCL21 greatly increases its effectiveness as an immunotherapy for neuroblastoma

Poelaert, Brittany J / Romanova, Svetlana / Knoche, Shelby M / Olson, Madeline T / Sliker, Bailee H / Smits, Kaitlin / Dickey, Brittney L / Moffitt-Holida, Alexandra E.J / Goetz, Benjamin T / Khan, Nuzhat / Smith, Lynette / Band, Hamid / Mohs, Aaron M / Coulter, Donald W / Bronich, Tatiana K / Solheim, Joyce C

Journal of controlled release. 2020 Nov. 10, v. 327

2020

Abstract	Neuroblastoma is the most commonly diagnosed extracranial solid tumor in children. The patients with aggressive metastatic disease or refractory/relapsed neuroblastoma currently face a dismally low chance of survival. Thus, there is a great need for more effective therapies for this illness. In previous studies, we, as well as others, showed that the immune cell chemoattractant C-C motif chemokine ligand 21 (CCL21) is effective as an intratumoral therapy able to slow the growth of cancers. In this current study, we developed and tested an injectable, slow-release, uniform, and optimally loaded alginate nanoformulation of CCL21 as a means to provide prolonged intratumoral treatment. The alginate-nanoformulated CCL21, when injected intratumorally into mice bearing neuroblastoma lesions, significantly prolonged survival and decreased the tumor growth rate compared to CCL21 alone, empty nanoparticles, or buffer. Notably, we also observed complete tumor clearance and subsequent full protection against tumor rechallenge in 33% of nanoformulated CCL21-treated mice. Greater intratumoral presence of nanoformulated CCL21, compared to free CCL21, at days 1 and 2 after treatment ended was confirmed through fluorescent labeling and tracking. Nanoformulated CCL21-treated tumors exhibited a general pattern of prolonged increases in anti-tumor cytokines and relatively lower levels of pro-tumor cytokines in comparison to tumors treated with CCL21 alone or buffer only. Thus, this novel nanoformulation of CCL21 is an effective treatment for neuroblastoma, and may have potential for the delivery of CCL21 to other types of solid tumors in the future and as a slow-release delivery modality for other immunotherapies
Keywords	alginates ; chemoattractants ; chemokine CCL21 ; children ; fluorescent labeling ; immunotherapy ; ligands ; metastasis ; mice ; nanoparticles ; neoplasms ; patients
Language	English
Dates of publication	2020-1110
Size	p. 266-283.
Publishing place	Elsevier B.V.
Document type	Article
ZDB-ID	632533-6
ISSN	1873-4995 ; 0168-3659
ISSN (online)	1873-4995
ISSN	0168-3659
DOI	10.1016/j.jconrel.2020.07.024
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Article ; Online: EHD1 and RUSC2 Control Basal Epidermal Growth Factor Receptor Cell Surface Expression and Recycling

Tom, Eric C. / Mushtaq, Insha / Mohapatra, Bhopal C. / Luan, Haitao / Bhat, Aaqib M. / Zutshi, Neha / Chakraborty, Sukanya / Islam, Namista / Arya, Priyanka / Bielecki, Timothy A. / Iseka, Fany M. / Bhattacharyya, Sohinee / Cypher, Luke R. / Goetz, Benjamin T. / Negi, Simarjeet K. / Storck, Matthew D. / Rana, Sandeep / Barnekow, Angelika / Singh, Pankaj K. /

Ying, Guoguang / Guda, Chittibabu / Natarajan, Amarnath / Band, Vimla / Band, Hamid

Molecular and Cellular Biology. 2020 Mar. 16, v. 40, no. 7 p.e00434-19-

2020

Abstract: Epidermal growth factor receptor (EGFR) is a prototype receptor tyrosine kinase and an oncoprotein in many solid tumors. Cell surface display of EGFR is essential for cellular responses to its ligands. While postactivation endocytic trafficking of EGFR ... ...

Abstract	Epidermal growth factor receptor (EGFR) is a prototype receptor tyrosine kinase and an oncoprotein in many solid tumors. Cell surface display of EGFR is essential for cellular responses to its ligands. While postactivation endocytic trafficking of EGFR has been well elucidated, little is known about mechanisms of basal/preactivation surface display of EGFR. Here, we identify a novel role of the endocytic regulator EHD1 and a potential EHD1 partner, RUSC2, in cell surface display of EGFR. EHD1 and RUSC2 colocalize with EGFR in vesicular/tubular structures and at the Golgi compartment. Inducible EHD1 knockdown reduced the cell surface EGFR expression with accumulation at the Golgi compartment, a phenotype rescued by exogenous EHD1. RUSC2 knockdown phenocopied the EHD1 depletion effects. EHD1 or RUSC2 depletion impaired the EGF-induced cell proliferation, demonstrating that the novel, EHD1- and RUSC2-dependent transport of unstimulated EGFR from the Golgi compartment to the cell surface that we describe is functionally important, with implications for physiologic and oncogenic roles of EGFR and targeted cancer therapies.
Keywords	cell proliferation ; epidermal growth factor receptors ; ligands ; oncogene proteins ; phenotype ; prototypes ; EGFR ; EHD1 ; endocytic trafficking
Language	English
Dates of publication	2020-0316
Publishing place	Taylor & Francis
Document type	Article ; Online
ZDB-ID	779397-2
ISSN	1098-5549 ; 0270-7306
ISSN (online)	1098-5549
ISSN	0270-7306
DOI	10.1128/MCB.00434-19
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Zs.A 1666: Show issues

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Article ; Online: EHD1 and RUSC2 Control Basal Epidermal Growth Factor Receptor Cell Surface Expression and Recycling.

Tom, Eric C / Mushtaq, Insha / Mohapatra, Bhopal C / Luan, Haitao / Bhat, Aaqib M / Zutshi, Neha / Chakraborty, Sukanya / Islam, Namista / Arya, Priyanka / Bielecki, Timothy A / Iseka, Fany M / Bhattacharyya, Sohinee / Cypher, Luke R / Goetz, Benjamin T / Negi, Simarjeet K / Storck, Matthew D / Rana, Sandeep / Barnekow, Angelika / Singh, Pankaj K /

Ying, Guoguang / Guda, Chittibabu / Natarajan, Amarnath / Band, Vimla / Band, Hamid

Molecular and cellular biology

2020 Volume 40, Issue 7

Abstract	Epidermal growth factor receptor (EGFR) is a prototype receptor tyrosine kinase and an oncoprotein in many solid tumors. Cell surface display of EGFR is essential for cellular responses to its ligands. While postactivation endocytic trafficking of EGFR has been well elucidated, little is known about mechanisms of basal/preactivation surface display of EGFR. Here, we identify a novel role of the endocytic regulator EHD1 and a potential EHD1 partner, RUSC2, in cell surface display of EGFR. EHD1 and RUSC2 colocalize with EGFR in vesicular/tubular structures and at the Golgi compartment. Inducible EHD1 knockdown reduced the cell surface EGFR expression with accumulation at the Golgi compartment, a phenotype rescued by exogenous EHD1. RUSC2 knockdown phenocopied the EHD1 depletion effects. EHD1 or RUSC2 depletion impaired the EGF-induced cell proliferation, demonstrating that the novel, EHD1- and RUSC2-dependent transport of unstimulated EGFR from the Golgi compartment to the cell surface that we describe is functionally important, with implications for physiologic and oncogenic roles of EGFR and targeted cancer therapies.
MeSH term(s)	Animals ; Carrier Proteins/metabolism ; Cell Communication/physiology ; Cell Line ; Cell Membrane/metabolism ; Cell Proliferation/physiology ; ErbB Receptors/metabolism ; Golgi Apparatus/metabolism ; Humans ; Mice ; Protein Transport/physiology ; RNA Interference ; RNA, Small Interfering/genetics ; Vesicular Transport Proteins/genetics ; Vesicular Transport Proteins/metabolism
Chemical Substances	Carrier Proteins ; EHD1 protein, human ; RNA, Small Interfering ; RUSC2 protein, human ; Vesicular Transport Proteins ; EGFR protein, human (EC 2.7.10.1) ; ErbB Receptors (EC 2.7.10.1)
Language	English
Publishing date	2020-03-16
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	779397-2
ISSN	1098-5549 ; 0270-7306
ISSN (online)	1098-5549
ISSN	0270-7306
DOI	10.1128/MCB.00434-19
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Article ; Online: CBL family E3 ubiquitin ligases control JAK2 ubiquitination and stability in hematopoietic stem cells and myeloid malignancies.

Lv, Kaosheng / Jiang, Jing / Donaghy, Ryan / Riling, Christopher R / Cheng, Ying / Chandra, Vemika / Rozenova, Krasimira / An, Wei / Mohapatra, Bhopal C / Goetz, Benjamin T / Pillai, Vinodh / Han, Xu / Todd, Emily A / Jeschke, Grace R / Langdon, Wallace Y / Kumar, Suresh / Hexner, Elizabeth O / Band, Hamid / Tong, Wei

Genes & development

2017 Volume 31, Issue 10, Page(s) 1007–1023

Abstract: Janus kinase 2 (JAK2) is a central kinase in hematopoietic stem/progenitor cells (HSPCs), and its uncontrolled activation is a prominent oncogenic driver of hematopoietic neoplasms. However, molecular mechanisms underlying the regulation of JAK2 have ... ...

Abstract	Janus kinase 2 (JAK2) is a central kinase in hematopoietic stem/progenitor cells (HSPCs), and its uncontrolled activation is a prominent oncogenic driver of hematopoietic neoplasms. However, molecular mechanisms underlying the regulation of JAK2 have remained elusive. Here we report that the Casitas B-cell lymphoma (CBL) family E3 ubiquitin ligases down-regulate JAK2 stability and signaling via the adaptor protein LNK/SH2B3. We demonstrated that depletion of
MeSH term(s)	Animals ; Cell Line, Tumor ; Cell Proliferation/genetics ; Cytokines/metabolism ; Enzyme Stability ; Hematopoietic Stem Cells/enzymology ; Humans ; Intracellular Signaling Peptides and Proteins/metabolism ; Janus Kinase 2/genetics ; Janus Kinase 2/metabolism ; Leukemia, Myeloid, Acute/enzymology ; Leukemia, Myeloid, Acute/genetics ; Leukemia, Myeloid, Acute/physiopathology ; Membrane Proteins ; Mice ; Mutation ; Proteolysis ; Proto-Oncogene Proteins c-cbl/genetics ; Proto-Oncogene Proteins c-cbl/metabolism ; Signal Transduction/genetics ; Ubiquitination
Chemical Substances	Cytokines ; Intracellular Signaling Peptides and Proteins ; Lnk protein, mouse ; Membrane Proteins ; Proto-Oncogene Proteins c-cbl (EC 2.3.2.27) ; Janus Kinase 2 (EC 2.7.10.2)
Language	English
Publishing date	2017-06-13
Publishing country	United States
Document type	Journal Article
ZDB-ID	806684-x
ISSN	1549-5477 ; 0890-9369
ISSN (online)	1549-5477
ISSN	0890-9369
DOI	10.1101/gad.297135.117
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Article ; Online: Role of the EHD Family of Endocytic Recycling Regulators for TCR Recycling and T Cell Function.

Iseka, Fany M / Goetz, Benjamin T / Mushtaq, Insha / An, Wei / Cypher, Luke R / Bielecki, Timothy A / Tom, Eric C / Arya, Priyanka / Bhattacharyya, Sohinee / Storck, Matthew D / Semerad, Craig L / Talmadge, James E / Mosley, R Lee / Band, Vimla / Band, Hamid

Journal of immunology (Baltimore, Md. : 1950)

2017 Volume 200, Issue 2, Page(s) 483–499

Abstract: T cells use the endocytic pathway for key cell biological functions, including receptor turnover and maintenance of the immunological synapse. Some of the established players include the Rab GTPases, the SNARE complex proteins, and others, which function ...

Abstract	T cells use the endocytic pathway for key cell biological functions, including receptor turnover and maintenance of the immunological synapse. Some of the established players include the Rab GTPases, the SNARE complex proteins, and others, which function together with EPS-15 homology domain-containing (EHD) proteins in non-T cell systems. To date, the role of the EHD protein family in T cell function remains unexplored. We generated conditional EHD1/3/4 knockout mice using CD4-Cre and crossed these with mice bearing a myelin oligodendrocyte glycoprotein-specific TCR transgene. We found that CD4
MeSH term(s)	Animals ; CD3 Complex/metabolism ; CD4-Positive T-Lymphocytes/immunology ; CD4-Positive T-Lymphocytes/metabolism ; Carrier Proteins/genetics ; DNA-Binding Proteins/genetics ; Encephalomyelitis, Autoimmune, Experimental/genetics ; Encephalomyelitis, Autoimmune, Experimental/immunology ; Encephalomyelitis, Autoimmune, Experimental/metabolism ; Endocytosis ; Female ; Gene Expression ; Gene Knockout Techniques ; Lymphocyte Activation ; Lymphoid Tissue/immunology ; Lymphoid Tissue/metabolism ; Lysosomes/metabolism ; Mice ; Mice, Knockout ; Multigene Family ; Multiprotein Complexes/metabolism ; Nuclear Proteins/genetics ; Protein Binding ; Protein Transport ; Proteolysis ; Receptors, Antigen, T-Cell/metabolism ; T-Lymphocytes/immunology ; T-Lymphocytes/metabolism ; Vesicular Transport Proteins/genetics ; Vesicular Transport Proteins/metabolism
Chemical Substances	CD3 Complex ; Carrier Proteins ; DNA-Binding Proteins ; EHD4 protein, mouse ; Ehd1 protein, mouse ; Ehd3 protein, mouse ; Multiprotein Complexes ; Nuclear Proteins ; Receptors, Antigen, T-Cell ; Vesicular Transport Proteins
Language	English
Publishing date	2017-12-06
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	3056-9
ISSN	1550-6606 ; 0022-1767 ; 1048-3233 ; 1047-7381
ISSN (online)	1550-6606
ISSN	0022-1767 ; 1048-3233 ; 1047-7381
DOI	10.4049/jimmunol.1601793
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