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Book ; Online: (Table S1) Chronostratigraphic constrains for sediment core AND1-1B, supplementary data to: Naish, Tim R; Powell, Ross; Levy, R; Wilson, Gary S; Scherer, Reed P; Talarico, Franco; Krissek, Lawrence A; Niessen, Frank; Pompilio, Massimo; Wilson, Terry; Carter, Lionel; DeConto, Robert M; Huybers, P; McKay, R; Pollard, David; Ross, J; Winter, Diane M; Barrett, Peter J; Browne, G; Cody, R; Cowan, Ellen A; Crampton, J; Dunbar, Gavin B; Dunbar, N; Florindo, Fabio; Gebhardt, Andrea Catalina; Graham, IJ; Hannah, Mike J; Hansaraj, D; Harwood, David M; Helling, D; Henrys, Stuart; Hinnov, L; Kuhn, Gerhard; Kyle, Philip R; Läufer, Andreas L; Maffioli, P; Magens, Diana; Mandernack, Kevin W; McIntosh, WC; Millan, C; Morin, Roger H; Ohneiser, Christian; Paulsen, Timothy S; Persico, Davide; Raine, J Ian; Reed, J; Riesselman, C; Sagnotti, Leo; Schmitt, D R; Sjunneskog, C; Strong, P; Taviani, Marco; Vogel, Stefan; Wilch, T; Williams, Trevor (2009): Obliquity-paced Pliocene West Antarctic ice sheet oscillations. Nature, 458(7236), 322-329

Naish, Tim R / Krissek, Lawrence A / Levy, R / Niessen, Frank / Pompilio, Massimo / Powell, Ross / Scherer, Reed P / Talarico, Franco / Wilson, Gary S / al., et

2009

Abstract: Thirty years after oxygen isotope records from microfossils deposited in ocean sediments confirmed the hypothesis that variations in the Earth's orbital geometry control the ice ages (Hays et al., 1976, doi:10.1126/science.194.4270.1121), fundamental ... ...

Abstract	Thirty years after oxygen isotope records from microfossils deposited in ocean sediments confirmed the hypothesis that variations in the Earth's orbital geometry control the ice ages (Hays et al., 1976, doi:10.1126/science.194.4270.1121), fundamental questions remain over the response of the Antarctic ice sheets to orbital cycles (Raymo and Huybers, 2008, doi:10.1038/nature06589). Furthermore, an understanding of the behaviour of the marine-based West Antarctic ice sheet (WAIS) during the 'warmer-than-present' early-Pliocene epoch (~5-3 Myr ago) is needed to better constrain the possible range of ice-sheet behaviour in the context of future global warming (Solomon et al., 2007). Here we present a marine glacial record from the upper 600 m of the AND-1B sediment core recovered from beneath the northwest part of the Ross ice shelf by the ANDRILL programme and demonstrate well-dated, ~40-kyr cyclic variations in ice-sheet extent linked to cycles in insolation influenced by changes in the Earth's axial tilt (obliquity) during the Pliocene. Our data provide direct evidence for orbitally induced oscillations in the WAIS, which periodically collapsed, resulting in a switch from grounded ice, or ice shelves, to open waters in the Ross embayment when planetary temperatures were up to ~3° C warmer than today ( Kim and Crowley, 2000, doi:10.1029/1999PA000459) and atmospheric CO2 concentration was as high as ~400 p.p.m.v. (van der Burgh et al., 1993, doi:10.1126/science.260.5115.1788, Raymo et al., 1996, doi:10.1016/0377-8398(95)00048-8). The evidence is consistent with a new ice-sheet/ice-shelf model (Pollard and DeConto, 2009, doi:10.1038/nature07809) that simulates fluctuations in Antarctic ice volume of up to +7 m in equivalent sea level associated with the loss of the WAIS and up to +3 m in equivalent sea level from the East Antarctic ice sheet, in response to ocean-induced melting paced by obliquity. During interglacial times, diatomaceous sediments indicate high surface-water productivity, minimal summer sea ice and air temperatures above freezing, suggesting an additional influence of surface melt (Huybers, 2006, doi:10.1126/science.1125249) under conditions of elevated CO2.
Language	English
Dates of publication	2009-9999
Size	Online-Ressource
Publisher	PANGAEA - Data Publisher for Earth & Environmental Science
Publishing place	Bremen/Bremerhaven
Document type	Book ; Online
Note	This dataset is supplement to doi:10.1038/nature07867
DOI	10.1594/PANGAEA.769658
Database	Library catalogue of the German National Library of Science and Technology (TIB), Hannover

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Article ; Online: Notch activation promotes endothelial survival through a PI3K-Slug axis.

Chang, Linda / Wong, Fred / Niessen, Kyle / Karsan, Aly

Microvascular research

2013 Volume 89, Page(s) 80–85

Abstract: Rationale: Loss of endothelial viability correlates with initiation and progress of vascular pathology. However, much remains to be learned about pathways required to maintain the balance between cell viability and apoptosis. Notch activation can ... ...

Abstract	Rationale: Loss of endothelial viability correlates with initiation and progress of vascular pathology. However, much remains to be learned about pathways required to maintain the balance between cell viability and apoptosis. Notch activation can enhance or inhibit apoptosis but its role in maintaining the endothelium needs further delineation. Objective: This study aims to identify the mechanisms by which Notch activation regulates endothelial viability. Methods and results: Endothelial cells transduced with active Notch were treated with lipopolysaccharide (LPS) or homocysteine to induce endothelial apoptosis. Notch protected against LPS-induced cell death but exacerbated homocysteine-induced apoptosis. Inhibition of PI3K revealed that ligand-induced activation of endogenous Notch initiates parallel death and survival pathways and exhibits a differential effect on endothelial survival depending on the apoptotic stimulus. PI3K activity regulated the expression of Slug, which was required for survival in Notch-activated endothelial cells. Homocysteine, but not LPS, blocked both PI3K activity and Slug expression in Notch-activated cells, leading to increased endothelial apoptosis. Conclusions: Notch signaling leads to activation of parallel survival and apoptotic pathways in endothelial cells. The interaction of Notch with other signaling pathways plays an important contextual role in regulating endothelial viability.
MeSH term(s)	Apoptosis ; Cell Survival ; Endothelial Cells/cytology ; Enzyme Inhibitors/chemistry ; Gene Expression Regulation ; Homocysteine/chemistry ; Humans ; Ligands ; Lipopolysaccharides/chemistry ; Microcirculation ; Microscopy, Fluorescence ; Phosphatidylinositol 3-Kinases/metabolism ; Receptors, Notch/metabolism ; Signal Transduction ; Snail Family Transcription Factors ; Time Factors ; Transcription Factors/metabolism
Chemical Substances	Enzyme Inhibitors ; Ligands ; Lipopolysaccharides ; Receptors, Notch ; SNAI1 protein, human ; Snail Family Transcription Factors ; Transcription Factors ; Homocysteine (0LVT1QZ0BA) ; Phosphatidylinositol 3-Kinases (EC 2.7.1.-)
Language	English
Publishing date	2013-09
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80307-8
ISSN	1095-9319 ; 0026-2862
ISSN (online)	1095-9319
ISSN	0026-2862
DOI	10.1016/j.mvr.2013.05.007
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Article ; Online: Bone marrow adipocytes fuel emergency hematopoiesis after myocardial infarction.

Zhang, Shuang / Paccalet, Alexandre / Rohde, David / Cremer, Sebastian / Hulsmans, Maarten / Lee, I-Hsiu / Mentkowski, Kyle / Grune, Jana / Schloss, Maximilian J / Honold, Lisa / Iwamoto, Yoshiko / Zheng, Yi / Bredella, Miriam A / Buckless, Colleen / Ghoshhajra, Brian / Thondapu, Vikas / van der Laan, Anja M / Piek, Jan J / Niessen, Hans W M /

Pallante, Fabio / Carnevale, Raimondo / Perrotta, Sara / Carnevale, Daniela / Iborra-Egea, Oriol / Muñoz-Guijosa, Christian / Galvez-Monton, Carolina / Bayes-Genis, Antoni / Vidoudez, Charles / Trauger, Sunia A / Scadden, David / Swirski, Filip K / Moskowitz, Michael A / Naxerova, Kamila / Nahrendorf, Matthias

Nature cardiovascular research

2023 Volume 2, Issue 12, Page(s) 1277–1290

Abstract: After myocardial infarction (MI), emergency hematopoiesis produces inflammatory myeloid cells that accelerate atherosclerosis and promote heart failure. Since the balance between glycolysis and mitochondrial metabolism regulates hematopoietic stem cell ... ...

Abstract	After myocardial infarction (MI), emergency hematopoiesis produces inflammatory myeloid cells that accelerate atherosclerosis and promote heart failure. Since the balance between glycolysis and mitochondrial metabolism regulates hematopoietic stem cell homeostasis, metabolic cues may influence emergency myelopoiesis. Here, we show in humans and female mice that hematopoietic progenitor cells increase fatty acid metabolism after MI. Blockade of fatty acid oxidation by deleting carnitine palmitoyltransferase (
Language	English
Publishing date	2023-12-05
Publishing country	England
Document type	Journal Article
ISSN	2731-0590
ISSN (online)	2731-0590
DOI	10.1038/s44161-023-00388-7
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Article ; Online: Notch signaling in cardiac development.

Niessen, Kyle / Karsan, Aly

Circulation research

2008 Volume 102, Issue 10, Page(s) 1169–1181

Abstract: The Notch signaling pathway has been demonstrated to play a critical role during mammalian cardiac development based on recent findings from gene-targeted mice. In addition, mutations in the Notch signaling pathway have been associated with human ... ...

Abstract	The Notch signaling pathway has been demonstrated to play a critical role during mammalian cardiac development based on recent findings from gene-targeted mice. In addition, mutations in the Notch signaling pathway have been associated with human congenital heart defects such as Alagille syndrome, bicuspid aortic valve disease, calcification of the heart valves, and ventricular septal defects. Recently, it was demonstrated that Notch activation in the endocardium regulates ventricular myocardial development and that the Notch downstream target genes Hey1 and Hey2 are required for the establishment of the atrioventricular canal myocardial boundary. The Notch pathway has previously been implicated in regulating endothelial-to-mesenchymal transition during development of the heart valves, and recent reports further dissect the role of individual Notch downstream target genes during this process. In addition, a role for the Notch pathway during cardiac neural crest cell development has been identified, which provides a potential mechanism for the findings seen in Alagille syndrome. This review focuses on recently reported findings that elucidate mechanisms regulated by the Notch pathway during ventricular, atrioventricular canal, and outflow tract development.
MeSH term(s)	Animals ; Gene Expression Regulation, Developmental ; Heart/embryology ; Heart/physiology ; Humans ; Receptors, Notch/genetics ; Receptors, Notch/metabolism ; Signal Transduction/physiology
Chemical Substances	Receptors, Notch
Language	English
Publishing date	2008-05-23
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	80100-8
ISSN	1524-4571 ; 0009-7330 ; 0931-6876
ISSN (online)	1524-4571
ISSN	0009-7330 ; 0931-6876
DOI	10.1161/CIRCRESAHA.108.174318
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Article: Notch signaling in the developing cardiovascular system.

Niessen, Kyle / Karsan, Aly

American journal of physiology. Cell physiology

2007 Volume 293, Issue 1, Page(s) C1–11

Abstract: The Notch proteins encompass a family of transmembrane receptors that have been highly conserved through evolution as mediators of cell fate. Recent findings have demonstrated a critical role of Notch in the developing cardiovascular system. Notch ... ...

Abstract	The Notch proteins encompass a family of transmembrane receptors that have been highly conserved through evolution as mediators of cell fate. Recent findings have demonstrated a critical role of Notch in the developing cardiovascular system. Notch signaling has been implicated in the endothelial-to-mesenchymal transition during development of the heart valves, in arterial-venous differentiation, and in remodeling of the primitive vascular plexus. Mutations of Notch pathway components in humans are associated with congenital defects of the cardiovascular system such as Alagille syndrome, cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL), and bicuspid aortic valves. This article focuses on the role of the Notch pathway in the developing cardiovascular system and congenital human cardiovascular diseases.
MeSH term(s)	Animals ; Arteries/embryology ; Arteries/metabolism ; Body Patterning ; Cardiovascular Abnormalities/genetics ; Cardiovascular Abnormalities/metabolism ; Cardiovascular System/embryology ; Cardiovascular System/metabolism ; Heart/embryology ; Humans ; Ligands ; Models, Cardiovascular ; Models, Molecular ; Molecular Conformation ; Mutation ; Myocardium/metabolism ; Receptors, Notch/chemistry ; Receptors, Notch/genetics ; Receptors, Notch/metabolism ; Signal Transduction ; Veins/embryology ; Veins/metabolism
Chemical Substances	Ligands ; Receptors, Notch
Language	English
Publishing date	2007-03-21
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	392098-7
ISSN	1522-1563 ; 0363-6143
ISSN (online)	1522-1563
ISSN	0363-6143
DOI	10.1152/ajpcell.00415.2006
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Article ; Online: Integrin αvβ8 on T cells suppresses anti-tumor immunity in multiple models and is a promising target for tumor immunotherapy.

Dodagatta-Marri, Eswari / Ma, Hsiao-Yen / Liang, Benjia / Li, John / Meyer, Dominique S / Chen, Szu-Ying / Sun, Kai-Hui / Ren, Xin / Zivak, Bahar / Rosenblum, Michael D / Headley, Mark B / Pinzas, Lauren / Reed, Nilgun I / Del Cid, Joselyn S / Hann, Byron C / Yang, Sharon / Giddabasappa, Anand / Noorbehesht, Kavon / Yang, Bing /

Dal Porto, Joseph / Tsukui, Tatsuya / Niessen, Kyle / Atakilit, Amha / Akhurst, Rosemary J / Sheppard, Dean

Cell reports

2021 Volume 36, Issue 1, Page(s) 109309

Abstract: αvβ8 integrin, a key activator of transforming growth factor β (TGF-β), inhibits anti-tumor immunity. We show that a potent blocking monoclonal antibody against αvβ8 (ADWA-11) causes growth suppression or complete regression in syngeneic models of ... ...

Abstract	αvβ8 integrin, a key activator of transforming growth factor β (TGF-β), inhibits anti-tumor immunity. We show that a potent blocking monoclonal antibody against αvβ8 (ADWA-11) causes growth suppression or complete regression in syngeneic models of squamous cell carcinoma, mammary cancer, colon cancer, and prostate cancer, especially when combined with other immunomodulators or radiotherapy. αvβ8 is expressed at the highest levels in CD4+CD25+ T cells in tumors, and specific deletion of β8 from T cells is as effective as ADWA-11 in suppressing tumor growth. ADWA-11 increases expression of a suite of genes in tumor-infiltrating CD8+ T cells normally inhibited by TGF-β and involved in tumor cell killing, including granzyme B and interferon-γ. The in vitro cytotoxic effect of tumor CD8 T cells is inhibited by CD4+CD25+ cells, and this suppressive effect is blocked by ADWA-11. These findings solidify αvβ8 integrin as a promising target for cancer immunotherapy.
MeSH term(s)	Animals ; Antibodies, Neoplasm/immunology ; CD4-Positive T-Lymphocytes/immunology ; CD8-Positive T-Lymphocytes/immunology ; CTLA-4 Antigen/immunology ; Cell Line, Tumor ; Cell Proliferation ; Gene Expression Regulation, Neoplastic ; Granzymes/metabolism ; Immunity ; Immunotherapy ; Integrins/metabolism ; Interferon-gamma/metabolism ; Lymphocyte Depletion ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Models, Biological ; Mutation/genetics ; Neoplasms/genetics ; Neoplasms/immunology ; Neoplasms/pathology ; Neoplasms/therapy ; Signal Transduction ; Smad3 Protein/metabolism ; Survival Analysis ; T-Lymphocytes/immunology ; T-Lymphocytes, Cytotoxic/immunology ; Transforming Growth Factor beta/metabolism ; Tumor Microenvironment/immunology ; Tumor Necrosis Factor Receptor Superfamily, Member 9/metabolism
Chemical Substances	Antibodies, Neoplasm ; CTLA-4 Antigen ; Integrins ; Smad3 Protein ; Transforming Growth Factor beta ; Tumor Necrosis Factor Receptor Superfamily, Member 9 ; integrin alphavbeta8 ; Interferon-gamma (82115-62-6) ; Granzymes (EC 3.4.21.-)
Language	English
Publishing date	2021-06-29
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.2021.109309
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Article ; Online: RUNX3 maintains the mesenchymal phenotype after termination of the Notch signal.

Fu, YangXin / Chang, Alex Chia Yu / Fournier, Michèle / Chang, Linda / Niessen, Kyle / Karsan, Aly

The Journal of biological chemistry

2011 Volume 286, Issue 13, Page(s) 11803–11813

Abstract: Notch is a critical mediator of endothelial-to-mesenchymal transition (EndMT) during cardiac cushion development. Slug, a transcriptional repressor that is a Notch target, is an important Notch effector of EndMT in the cardiac cushion. Here, we report ... ...

Abstract	Notch is a critical mediator of endothelial-to-mesenchymal transition (EndMT) during cardiac cushion development. Slug, a transcriptional repressor that is a Notch target, is an important Notch effector of EndMT in the cardiac cushion. Here, we report that the runt-related transcription factor RUNX3 is a novel direct Notch target in the endothelium. Ectopic expression of RUNX3 in endothelium induces Slug expression and EndMT independent of Notch activation. Interestingly, RUNX3 physically interacts with CSL, the Notch-interacting partner in the nucleus, and induces Slug in a CSL-dependent, but Notch-independent manner. Although RUNX3 may not be required for the initial induction of Slug and EndMT by Notch, because RUNX3 has a much longer half-life than Slug, it sustains the expression of Slug thereby maintaining the mesenchymal phenotype. CSL binds to the Runx3 promoter in the atrioventricular canal in vivo, and inhibition of Notch reduces RUNX3 expression in the cardiac cushion of embryonic hearts. Taken together, our results suggest that induction of RUNX3 may be a mechanism to maintain Notch-transformed mesenchymal cells during heart development.
MeSH term(s)	Cell Line ; Core Binding Factor Alpha 3 Subunit/genetics ; Core Binding Factor Alpha 3 Subunit/metabolism ; Embryo, Mammalian/cytology ; Embryo, Mammalian/embryology ; Endothelium/embryology ; Epithelial-Mesenchymal Transition/physiology ; Gene Expression Regulation, Developmental/physiology ; Half-Life ; Heart/embryology ; Humans ; Mesoderm/cytology ; Mesoderm/metabolism ; Organogenesis/physiology ; Promoter Regions, Genetic/physiology ; Receptors, Notch/genetics ; Receptors, Notch/metabolism ; Snail Family Transcription Factors ; Transcription Factors/biosynthesis ; Transcription Factors/genetics
Chemical Substances	Core Binding Factor Alpha 3 Subunit ; Receptors, Notch ; Runx3 protein, human ; SNAI1 protein, human ; Snail Family Transcription Factors ; Transcription Factors
Language	English
Publishing date	2011-02-02
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2997-x
ISSN	1083-351X ; 0021-9258
ISSN (online)	1083-351X
ISSN	0021-9258
DOI	10.1074/jbc.M111.222331
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Article ; Online: Notch initiates the endothelial-to-mesenchymal transition in the atrioventricular canal through autocrine activation of soluble guanylyl cyclase.

Chang, Alex C Y / Fu, YangXin / Garside, Victoria C / Niessen, Kyle / Chang, Linda / Fuller, Megan / Setiadi, Audi / Smrz, Justin / Kyle, Alastair / Minchinton, Andrew / Marra, Marco / Hoodless, Pamela A / Karsan, Aly

Developmental cell

2011 Volume 21, Issue 2, Page(s) 288–300

Abstract: The heart is the most common site of congenital defects, and valvuloseptal defects are the most common of the cardiac anomalies seen in the newborn. The process of endothelial-to-mesenchymal transition (EndMT) in the cardiac cushions is a required step ... ...

Abstract	The heart is the most common site of congenital defects, and valvuloseptal defects are the most common of the cardiac anomalies seen in the newborn. The process of endothelial-to-mesenchymal transition (EndMT) in the cardiac cushions is a required step during early valve development, and Notch signaling is required for this process. Here we show that Notch activation induces the transcription of both subunits of the soluble guanylyl cyclase (sGC) heterodimer, GUCY1A3 and GUCY1B3, which form the nitric oxide receptor. In parallel, Notch also promotes nitric oxide (NO) production by inducing Activin A, thereby activating a PI3-kinase/Akt pathway to phosphorylate eNOS. We thus show that the activation of sGC by NO through a Notch-dependent autocrine loop is necessary to drive early EndMT in the developing atrioventricular canal (AVC).
MeSH term(s)	Animals ; Cells, Cultured ; Chromatin Immunoprecipitation/methods ; Endocardial Cushions/cytology ; Endothelium/physiology ; Female ; Gene Expression Profiling/methods ; Guanylate Cyclase/metabolism ; Male ; Mesoderm/physiology ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Nitric Oxide Synthase Type III/deficiency ; Oligonucleotide Array Sequence Analysis/methods ; RNA Interference/physiology ; Receptors, Cytoplasmic and Nuclear/metabolism ; Receptors, Notch/metabolism ; Signal Transduction ; Soluble Guanylyl Cyclase
Chemical Substances	Gucy1a3 protein, mouse ; Gucy1b3 protein, mouse ; Receptors, Cytoplasmic and Nuclear ; Receptors, Notch ; Nitric Oxide Synthase Type III (EC 1.14.13.39) ; Guanylate Cyclase (EC 4.6.1.2) ; Soluble Guanylyl Cyclase (EC 4.6.1.2)
Language	English
Publishing date	2011-08-16
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2054967-2
ISSN	1878-1551 ; 1534-5807
ISSN (online)	1878-1551
ISSN	1534-5807
DOI	10.1016/j.devcel.2011.06.022
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Zs.A 5742: 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)
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Article: An enzyme that regulates ether lipid signaling pathways in cancer annotated by multidimensional profiling.

Chiang, Kyle P / Niessen, Sherry / Saghatelian, Alan / Cravatt, Benjamin F

Chemistry & biology

2006 Volume 13, Issue 10, Page(s) 1041–1050

Abstract: Hundreds, if not thousands, of uncharacterized enzymes currently populate the human proteome. Assembly of these proteins into the metabolic and signaling pathways that govern cell physiology and pathology constitutes a grand experimental challenge. Here, ...

Abstract	Hundreds, if not thousands, of uncharacterized enzymes currently populate the human proteome. Assembly of these proteins into the metabolic and signaling pathways that govern cell physiology and pathology constitutes a grand experimental challenge. Here, we address this problem by using a multidimensional profiling strategy that combines activity-based proteomics and metabolomics. This approach determined that KIAA1363, an uncharacterized enzyme highly elevated in aggressive cancer cells, serves as a central node in an ether lipid signaling network that bridges platelet-activating factor and lysophosphatidic acid. Biochemical studies confirmed that KIAA1363 regulates this pathway by hydrolyzing the metabolic intermediate 2-acetyl monoalkylglycerol. Inactivation of KIAA1363 disrupted ether lipid metabolism in cancer cells and impaired cell migration and tumor growth in vivo. The integrated molecular profiling method described herein should facilitate the functional annotation of metabolic enzymes in any living system.
MeSH term(s)	Carbamates/chemistry ; Carbamates/pharmacology ; Carboxylic Ester Hydrolases/antagonists & inhibitors ; Carboxylic Ester Hydrolases/chemistry ; Carboxylic Ester Hydrolases/metabolism ; Cell Line, Tumor ; Chromatography, High Pressure Liquid/methods ; Enzyme Activation/drug effects ; Enzyme Inhibitors/chemistry ; Enzyme Inhibitors/pharmacology ; Female ; Humans ; Ketones/chemistry ; Ketones/pharmacology ; Lysophospholipids/chemistry ; Lysophospholipids/metabolism ; Ovarian Neoplasms/enzymology ; Ovarian Neoplasms/metabolism ; Phospholipid Ethers/chemistry ; Phospholipid Ethers/metabolism ; Platelet Activating Factor/metabolism ; RNA Interference ; Sensitivity and Specificity ; Signal Transduction/drug effects
Chemical Substances	11-hexadecenyl trifluoromethyl ketone ; AS 115 ; Carbamates ; Enzyme Inhibitors ; Ketones ; Lysophospholipids ; Phospholipid Ethers ; Platelet Activating Factor ; Carboxylic Ester Hydrolases (EC 3.1.1.-) ; NCEH1 protein, human (EC 3.1.1.13)
Language	English
Publishing date	2006-07-01
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	917827-2
ISSN	1879-1301 ; 1074-5521
ISSN (online)	1879-1301
ISSN	1074-5521
DOI	10.1016/j.chembiol.2006.08.008
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Article ; Online: ALK1 signaling regulates early postnatal lymphatic vessel development.

Niessen, Kyle / Zhang, Gu / Ridgway, John Brady / Chen, Hao / Yan, Minhong

Blood

2009 Volume 115, Issue 8, Page(s) 1654–1661

Abstract: In vertebrates, endothelial cells form 2 hierarchical tubular networks, the blood vessels and the lymphatic vessels. Despite the difference in their structure and function and genetic programs that dictate their morphogenesis, common signaling pathways ... ...

Abstract	In vertebrates, endothelial cells form 2 hierarchical tubular networks, the blood vessels and the lymphatic vessels. Despite the difference in their structure and function and genetic programs that dictate their morphogenesis, common signaling pathways have been recognized that regulate both vascular systems. ALK1 is a member of the transforming growth factor-beta type I family of receptors, and compelling genetic evidence suggests its essential role in regulating blood vascular development. Here we report that ALK1 signaling is intimately involved in lymphatic development. Lymphatic endothelial cells express key components of the ALK1 pathway and respond robustly to ALK1 ligand stimulation in vitro. Blockade of ALK1 signaling results in defective lymphatic development in multiple organs of neonatal mice. We find that ALK1 signaling regulates the differentiation of lymphatic endothelial cells to influence the lymphatic vascular development and remodeling. Furthermore, simultaneous inhibition of ALK1 pathway increases apoptosis in lymphatic vessels caused by blockade of VEGFR3 signaling. Thus, our study reveals a novel aspect of ALK1 signaling in regulating lymphatic development and suggests that targeting ALK1 pathway might provide additional control of lymphangiogenesis in human diseases.
MeSH term(s)	Activin Receptors, Type I/metabolism ; Activin Receptors, Type II/metabolism ; Animals ; Animals, Newborn ; Apoptosis/physiology ; Cell Differentiation/physiology ; Cells, Cultured ; Endothelial Cells/metabolism ; Humans ; Ligands ; Lymphangiogenesis/physiology ; Lymphatic Vessels/metabolism ; Mice ; Signal Transduction ; Vascular Endothelial Growth Factor Receptor-3/antagonists & inhibitors ; Vascular Endothelial Growth Factor Receptor-3/metabolism
Chemical Substances	Ligands ; Vascular Endothelial Growth Factor Receptor-3 (EC 2.7.10.1) ; ACVRL1 protein, human (EC 2.7.11.30) ; Activin Receptors, Type I (EC 2.7.11.30) ; Activin Receptors, Type II (EC 2.7.11.30) ; Acvrl1 protein, mouse (EC 2.7.11.30)
Language	English
Publishing date	2009-11-10
Publishing country	United States
Document type	Journal Article
ZDB-ID	80069-7
ISSN	1528-0020 ; 0006-4971
ISSN (online)	1528-0020
ISSN	0006-4971
DOI	10.1182/blood-2009-07-235655
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Uh III Zs.140: 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)
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