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Article: Testicular fat deposition attenuates reproductive performance via decreased follicle-stimulating hormone level and sperm meiosis and testosterone synthesis in mouse.

Du, Miao / Chen, Shikun / Chen, Yang / Yuan, Xinxu / Dong, Huansheng

Animal bioscience

2023 Volume 37, Issue 1, Page(s) 50–60

Abstract: Objective: Testicular fat deposition has been reported to affect animal reproduction. However, the underlying mechanism remains poorly understood. The present study explored whether sperm meiosis and testosterone synthesis contribute to mouse testicular ...

Abstract	Objective: Testicular fat deposition has been reported to affect animal reproduction. However, the underlying mechanism remains poorly understood. The present study explored whether sperm meiosis and testosterone synthesis contribute to mouse testicular fat depositioninduced reproductive performance. Methods: High fat diet (HFD)-induced obesity CD1 mice (DIO) were used as a testicular fat deposition model. The serum hormone test was performed by agent kit. The quality of sperm was assessed using a Sperm Class Analyzer. Testicular tissue morphology was analyzed by histochemical methods. The expression of spermatocyte marker molecules was monitored by an immuno-fluorescence microscope during meiosis. Analysis of the synthesis of testosterone was performed by real-time polymerase chain reaction and reagent kit. Results: It was found that there was a significant increase in body weight among DIO mice, however, the food intake showed no difference compared to control mice fed a normal diet (CTR). The number of offspring in DIO mice decreased, but there was no significant difference from the CTR group. The levels of follicle-stimulating hormone were lower in DIO mice and their luteinizing hormone levels were similar. The results showed a remarkable decrease in sperm density and motility among DIO mice. We also found that fat accumulation affected the meiosis process, mainly reflected in the cross-exchange of homologous chromosomes. In addition, overweight increased fat deposition in the testis and reduced the expression of testosterone synthesis-related enzymes, thereby affecting the synthesis and secretion of testosterone by testicular Leydig cells. Conclusion: Fat accumulation in the testes causes testicular cell dysfunction, which affects testosterone hormone synthesis and ultimately affects sperm formation.
Language	English
Publishing date	2023-08-28
Publishing country	Korea (South)
Document type	Journal Article
ISSN	2765-0189
ISSN	2765-0189
DOI	10.5713/ab.23.0175
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Article ; Online: Contribution of Hepatic Steatosis-Intensified Extracellular Vesicle Release to Aggravated Inflammatory Endothelial Injury in Liver-Specific Asah1 Gene Knockout Mice.

Yuan, Xinxu / Bhat, Owais M / Zou, Yao / Zhang, Yang / Li, Pin-Lan

The American journal of pathology

2023 Volume 193, Issue 4, Page(s) 493–508

Abstract: To study the mechanism by which nonalcoholic fatty liver disease (NAFLD) contributes to vascular endothelial Nod-like receptor pyrin domain 3 (NLRP3) inflammasome activation and neointima hyperplasia, NAFLD was established in high-fat diet (HFD)-treated ... ...

Abstract	To study the mechanism by which nonalcoholic fatty liver disease (NAFLD) contributes to vascular endothelial Nod-like receptor pyrin domain 3 (NLRP3) inflammasome activation and neointima hyperplasia, NAFLD was established in high-fat diet (HFD)-treated Asah1
MeSH term(s)	Mice ; Animals ; Inflammasomes/metabolism ; Non-alcoholic Fatty Liver Disease/metabolism ; NLR Family, Pyrin Domain-Containing 3 Protein/genetics ; NLR Family, Pyrin Domain-Containing 3 Protein/metabolism ; Mice, Knockout ; Acid Ceramidase/genetics ; Acid Ceramidase/metabolism ; Endothelial Cells/metabolism ; Neointima/metabolism ; Gene Knockout Techniques ; Hyperplasia ; Liver/metabolism ; Extracellular Vesicles/metabolism ; Ceramides ; Diet, High-Fat/adverse effects ; Mice, Inbred C57BL
Chemical Substances	Inflammasomes ; NLR Family, Pyrin Domain-Containing 3 Protein ; Acid Ceramidase (EC 3.5.1.23) ; Ceramides ; Asah1 protein, mouse (EC 3.5.1.23)
Language	English
Publishing date	2023-01-10
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2943-9
ISSN	1525-2191 ; 0002-9440
ISSN (online)	1525-2191
ISSN	0002-9440
DOI	10.1016/j.ajpath.2022.12.007
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Article ; Online: MSCFS: inferring circRNA functional similarity based on multiple data sources.

Shu, Liang / Zhou, Cheng / Yuan, Xinxu / Zhang, Jingpu / Deng, Lei

BMC bioinformatics

2021 Volume 22, Issue Suppl 10, Page(s) 371

Abstract: Background: More and more evidence shows that circRNA plays an important role in various biological processes and human health. Therefore, inferring the circRNA's potential functions and obtaining circRNA functional similarity has become more and more ... ...

Abstract	Background: More and more evidence shows that circRNA plays an important role in various biological processes and human health. Therefore, inferring the circRNA's potential functions and obtaining circRNA functional similarity has become more and more significant. However, there is no effective approach to explore the functional similarity of circRNAs. Methods: In this paper, we propose a new approach, called MSCFS, to calculate the functional similarity of circRNA by integrating multiple data sources. We combine circRNA-disease association, circRNA-gene-Gene Ontology association, and circRNA sequence information to explore the functional similarity of circRNA. Firstly, we employ different learning representation methods from three data sources to establish three circRNA functional similarity networks. Then we integrate the three networks to obtain the final circRNA functional similarity. Results: We utilize circRNA-miRNA association similarity and circRNA co-expression similarity to evaluate the performance of MSCFS. The results show a positive correlation with miRNA association ([Formula: see text]) and circRNA co-expression similarity ([Formula: see text]). Finally, we construct a circRNA functional similarity network and perform case analysis. The result shows our method can be applied to infer new potential functions of circRNA and other associations. Conclusions: MSCFS combines multiple data sources related to circRNA functions. Correlation analysis and case analyses prove that MSCFS is a useful method to explore circRNA functional similarity.
MeSH term(s)	Gene Ontology ; Humans ; Information Storage and Retrieval ; MicroRNAs ; RNA, Circular
Chemical Substances	MicroRNAs ; RNA, Circular
Language	English
Publishing date	2021-07-16
Publishing country	England
Document type	Journal Article
ZDB-ID	2041484-5
ISSN	1471-2105 ; 1471-2105
ISSN (online)	1471-2105
ISSN	1471-2105
DOI	10.1186/s12859-021-04287-1
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Article ; Online: Regulatory role of mammalian target of rapamycin signaling in exosome secretion and osteogenic changes in smooth muscle cells lacking acid ceramidase gene.

Bhat, Owais M / Yuan, Xinxu / Kukreja, Rakesh C / Li, Pin-Lan

FASEB journal : official publication of the Federation of American Societies for Experimental Biology

2021 Volume 35, Issue 7, Page(s) e21732

Abstract: Acid ceramidase (murine gene code: Asah1) (50 kDa) belongs to N-terminal nucleophile hydrolase family. This enzyme is located in the lysosome, which mediates conversion of ceramide (CER) into sphingosine and free fatty acids at acidic pH. CER plays an ... ...

Abstract	Acid ceramidase (murine gene code: Asah1) (50 kDa) belongs to N-terminal nucleophile hydrolase family. This enzyme is located in the lysosome, which mediates conversion of ceramide (CER) into sphingosine and free fatty acids at acidic pH. CER plays an important role in intracellular sphingolipid metabolism and its increase causes inflammation. The mammalian target of rapamycin complex 1 (mTORC1) signaling on late endosomes (LEs)/lysosomes may control cargo selection, membrane biogenesis, and exosome secretion, which may be fine controlled by lysosomal sphingolipids such as CER. This lysosomal-CER-mTOR signaling may be a crucial molecular mechanism responsible for development of arterial medial calcification (AMC). Torin-1 (5 mg/kg/day), an mTOR inhibitor, significantly decreased aortic medial calcification accompanied with decreased expression of osteogenic markers like osteopontin (OSP) and runt-related transcription factor 2 (RUNX2) and upregulation of smooth muscle 22α (SM22-α) in mice receiving high dose of Vitamin D (500 000 IU/kg/day). Asah1
MeSH term(s)	Acid Ceramidase/metabolism ; Animals ; Aorta/metabolism ; Calcium/metabolism ; Ceramides/metabolism ; Core Binding Factor Alpha 1 Subunit/metabolism ; Coronary Vessels/metabolism ; Exosomes/metabolism ; Lysosomes/metabolism ; Male ; Mammals/metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Multivesicular Bodies/metabolism ; Myocytes, Smooth Muscle/metabolism ; Osteogenesis/physiology ; Pulse Wave Analysis/methods ; Signal Transduction/physiology ; Sirolimus/metabolism ; Sphingolipids/metabolism ; TOR Serine-Threonine Kinases/metabolism ; Vascular Calcification/metabolism
Chemical Substances	Ceramides ; Core Binding Factor Alpha 1 Subunit ; Sphingolipids ; TOR Serine-Threonine Kinases (EC 2.7.11.1) ; Acid Ceramidase (EC 3.5.1.23) ; Asah1 protein, mouse (EC 3.5.1.23) ; Calcium (SY7Q814VUP) ; Sirolimus (W36ZG6FT64)
Language	English
Publishing date	2021-07-03
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	639186-2
ISSN	1530-6860 ; 0892-6638
ISSN (online)	1530-6860
ISSN	0892-6638
DOI	10.1096/fj.202100385R
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Zs.A 2266: 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)
Zs.MO 296: Show issues

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Article: Regulation of exosome release by lysosomal acid ceramidase in coronary arterial endothelial cells: Role of TRPML1 channel.

Li, Guangbi / Huang, Dandan / Li, Pengyang / Yuan, Xinxu / Yarotskyy, Viktor / Li, Pin-Lan

Current topics in membranes

2022 Volume 90, Page(s) 37–63

Abstract: Lysosomal acid ceramidase (AC) has been reported to determine multivesicular body (MVB) fate and exosome secretion in different mammalian cells including coronary arterial endothelial cells (CAECs). However, this AC-mediated regulation of exosome release ...

Abstract	Lysosomal acid ceramidase (AC) has been reported to determine multivesicular body (MVB) fate and exosome secretion in different mammalian cells including coronary arterial endothelial cells (CAECs). However, this AC-mediated regulation of exosome release from CAECs and associated underlying mechanism remain poorly understood. In the present study, we hypothesized that AC controls lysosomal Ca
MeSH term(s)	Mice ; Animals ; Acid Ceramidase/genetics ; Acid Ceramidase/metabolism ; Exosomes/metabolism ; Endothelial Cells/metabolism ; Transient Receptor Potential Channels/metabolism ; Sphingosine/metabolism ; Lysosomes/metabolism ; Mice, Knockout ; Mammals/metabolism
Chemical Substances	Acid Ceramidase (EC 3.5.1.23) ; Transient Receptor Potential Channels ; Sphingosine (NGZ37HRE42)
Language	English
Publishing date	2022-10-03
Publishing country	United States
Document type	Journal Article
ISSN	1063-5823
ISSN	1063-5823
DOI	10.1016/bs.ctm.2022.09.002
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Article ; Online: Endothelial Acid Sphingomyelinase Promotes NLRP3 Inflammasome and Neointima Formation During Hypercholesterolemia.

Yuan, Xinxu / Bhat, Owais M / Zou, Yao / Li, Xiang / Zhang, Yang / Li, Pin-Lan

Journal of lipid research

2022 Volume 63, Issue 12, Page(s) 100298

Abstract: The NOD-like receptor pyrin domain 3 (NLRP3) inflammasome is activated during atherogenesis, but how this occurs is unclear. Here, we explored the mechanisms activating and regulating NLRP3 inflammasomes via the acid sphingomyelinase (ASM)-ceramide ... ...

Abstract	The NOD-like receptor pyrin domain 3 (NLRP3) inflammasome is activated during atherogenesis, but how this occurs is unclear. Here, we explored the mechanisms activating and regulating NLRP3 inflammasomes via the acid sphingomyelinase (ASM)-ceramide signaling pathway. As a neointima formation model, partial left carotid ligations were performed on endothelial cell (EC)-specific ASM transgene mice (Smpd1
MeSH term(s)	Animals ; Mice ; Inflammasomes/metabolism ; NLR Family, Pyrin Domain-Containing 3 Protein/genetics ; NLR Family, Pyrin Domain-Containing 3 Protein/metabolism ; Hypercholesterolemia ; NLR Proteins ; Superoxides/metabolism ; Sphingomyelin Phosphodiesterase/genetics ; Sphingomyelin Phosphodiesterase/metabolism ; Neointima/metabolism ; Pyrin Domain ; Ceramides ; Caspases/metabolism ; Interleukin-1beta/metabolism
Chemical Substances	Inflammasomes ; NLR Family, Pyrin Domain-Containing 3 Protein ; NLR Proteins ; Superoxides (11062-77-4) ; Sphingomyelin Phosphodiesterase (EC 3.1.4.12) ; Ceramides ; Caspases (EC 3.4.22.-) ; Interleukin-1beta ; Nlrp3 protein, mouse
Language	English
Publishing date	2022-10-15
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	80154-9
ISSN	1539-7262 ; 0022-2275
ISSN (online)	1539-7262
ISSN	0022-2275
DOI	10.1016/j.jlr.2022.100298
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Article ; Online: Renomedullary exosomes produce antihypertensive effects in reversible two-kidney one-clip renovascular hypertensive mice.

Hu, Gaizun / Li, Guangbi / Huang, Dandan / Zou, Yao / Yuan, Xinxu / Ritter, Joseph K / Li, Ningjun / Li, Pin-Lan

Biochemical pharmacology

2022 Volume 204, Page(s) 115238

Abstract: The rapid fall in blood pressure following unclipping of the stenotic renal artery in the Goldblatt two-kidney one-clip (2K1C) model of renovascular hypertension is proposed to be due to release of renomedullary vasodepressor lipids, but the mechanism ... ...

Abstract	The rapid fall in blood pressure following unclipping of the stenotic renal artery in the Goldblatt two-kidney one-clip (2K1C) model of renovascular hypertension is proposed to be due to release of renomedullary vasodepressor lipids, but the mechanism has remained unclear. In this study, we hypothesized that the hypotensive response to unclipping is mediated by exosomes released from the renal medulla. In male C57BL6/J mice made hypertensive by the 2K1C surgery, unclipping of the renal artery after 10 days decreased mean arterial pressure (MAP) by 23 mmHg one hr after unclipping. This effect was accompanied by a 556% increase in the concentration of exosomes in plasma as observed by nanoparticle tracking analysis. Immunohistochemical analysis of exosome markers, CD63 and AnnexinII, showed increased staining in interstitial cells of the inner medulla of stenotic but not contralateral control kidney of clipped 2K1C mice. Treatment with rapamycin, an inducer of exosome release, blunted the hypertensive response to clipping, whereas GW-4869, an exosome biosynthesis inhibitor, prevented both the clipping-induced increase in inner medullary exosome marker staining and the unclipping-induced fall in MAP. Plasma exosomes isolated from unclipped 2K1C mice showed elevated neutral lipid content compared to sham mouse exosomes by flow cytometric analysis after Nile red staining. Exosomes from 2K1C but not sham control mice exerted potent MAP-lowering and diuretic-natriuretic effects in both 2K1C and angiotensin II-infused hypertensive mice. These results are consistent with increased renomedullary synthesis and release of exosomes with elevated antihypertensive neutral lipids in response to increased renal perfusion pressure.
MeSH term(s)	Angiotensin II/pharmacology ; Animals ; Antihypertensive Agents/pharmacology ; Antihypertensive Agents/therapeutic use ; Blood Pressure ; Diuretics/pharmacology ; Exosomes ; Hypertension/therapy ; Kidney ; Lipids ; Male ; Mice ; Natriuretic Agents/pharmacology ; Sirolimus/pharmacology
Chemical Substances	Antihypertensive Agents ; Diuretics ; Lipids ; Natriuretic Agents ; Angiotensin II (11128-99-7) ; Sirolimus (W36ZG6FT64)
Language	English
Publishing date	2022-08-31
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	208787-x
ISSN	1873-2968 ; 0006-2952
ISSN (online)	1873-2968
ISSN	0006-2952
DOI	10.1016/j.bcp.2022.115238
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Zs.A 19: Show issues

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Article: Downregulation of Lysosomal Acid Ceramidase Mediates HMGB1-Induced Migration and Proliferation of Mouse Coronary Arterial Myocytes.

Yuan, Xinxu / Bhat, Owais M / Lohner, Hannah / Zhang, Yang / Li, Pin-Lan

Frontiers in cell and developmental biology

2020 Volume 8, Page(s) 111

Abstract: High-mobility group box 1 protein (HMGB1) has been reported to trigger lysosome destabilization causing a wide of inflammatory diseases. The present study tested whether a lysosomal enzyme, acid ceramidase (AC), plays a critical role in HMGB1-induced ... ...

Abstract	High-mobility group box 1 protein (HMGB1) has been reported to trigger lysosome destabilization causing a wide of inflammatory diseases. The present study tested whether a lysosomal enzyme, acid ceramidase (AC), plays a critical role in HMGB1-induced alteration in ceramide metabolism and whether such HMGB1-AC interaction is associated with abnormal migration and proliferation of vascular smooth muscle cells (SMCs). We first observed that the expression of AC in the medial layer of mouse coronary arterial wall and colocalization of AC with a lysosome marker Lamp-1. In primary cultured coronary arterial myocytes (CAMs), AC expression and colocalization with Lamp-1 were significantly up-regulated by AC inducer, genistein, but down-regulated by AC inhibitor, N-oleoylethanolamine (NOE). HMGB1 dose-dependently decreased the colocalization of AC with Lamp-1 and reduced mRNA and protein expressions of AC in CAMs, but reversed by genistein. Consistently, HMGB1 significantly induced increases in the levels of long-chain ceramides in CAMs, which were not further enhanced by NOE but blocked by genistein. More importantly, HMGB1 promoted migration and proliferation of CAMs, which were not further increased by NOE but reduced by genistein. Lastly, CAMs isolated from smooth muscle-specific AC knockout mice (AC gene
Language	English
Publishing date	2020-03-10
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2737824-X
ISSN	2296-634X
ISSN	2296-634X
DOI	10.3389/fcell.2020.00111
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Article: Reversal of Endothelial Extracellular Vesicle-Induced Smooth Muscle Phenotype Transition by Hypercholesterolemia Stimulation: Role of NLRP3 Inflammasome Activation.

Yuan, Xinxu / Bhat, Owais M / Samidurai, Arun / Das, Anindita / Zhang, Yang / Li, Pin-Lan

Frontiers in cell and developmental biology

2020 Volume 8, Page(s) 597423

Abstract: Recent studies reported that vascular endothelial cells (ECs) secrete NLR family pyrin domain-containing 3 (NLRP3) inflammasome products such as interleukin-1β (IL-1β) via extracellular vesicles (EVs) under various pathological conditions. EVs represent ... ...

Abstract	Recent studies reported that vascular endothelial cells (ECs) secrete NLR family pyrin domain-containing 3 (NLRP3) inflammasome products such as interleukin-1β (IL-1β) via extracellular vesicles (EVs) under various pathological conditions. EVs represent one of the critical mechanisms mediating the cell-to-cell communication between ECs and vascular smooth muscle cells (VSMCs). However, whether or not the inflammasome-dependent EVs directly participate in the regulation of VSMC function remains unknown. In the present study, we found that in cultured carotid ECs, atherogenic stimulation by oxysterol 7-ketocholesterol (7-Ket) induced NLRP3 inflammasome formation and activation, reduced lysosome-multivesicular bodies (MVBs) fusion, and increased secretion of EVs that contain inflammasome product IL-1β. These EC-derived IL-1β-containing EVs promoted synthetic phenotype transition of co-cultured VSMCs, whereas EVs from unstimulated ECs have the opposite effects. Moreover, acid ceramidase
Language	English
Publishing date	2020-12-21
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2737824-X
ISSN	2296-634X
ISSN	2296-634X
DOI	10.3389/fcell.2020.597423
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Article ; Online: Abnormal Lysosomal Positioning and Small Extracellular Vesicle Secretion in Arterial Stiffening and Calcification of Mice Lacking Mucolipin 1 Gene.

Bhat, Owais M / Yuan, Xinxu / Camus, Sarah / Salloum, Fadi N / Li, Pin-Lan

International journal of molecular sciences

2020 Volume 21, Issue 5

Abstract: Recent studies have shown that arterial medial calcification is mediated by abnormal release of exosomes/small extracellular vesicles from vascular smooth muscle cells (VSMCs) and that small extracellular vesicle (sEV) secretion from cells is associated ... ...

Abstract	Recent studies have shown that arterial medial calcification is mediated by abnormal release of exosomes/small extracellular vesicles from vascular smooth muscle cells (VSMCs) and that small extracellular vesicle (sEV) secretion from cells is associated with lysosome activity. The present study was designed to investigate whether lysosomal expression of mucolipin-1, a product of the mouse
MeSH term(s)	Animals ; Core Binding Factor Alpha 1 Subunit/genetics ; Core Binding Factor Alpha 1 Subunit/metabolism ; Extracellular Vesicles/metabolism ; Extracellular Vesicles/pathology ; Immunohistochemistry ; Lysosomal-Associated Membrane Protein 1/genetics ; Lysosomal-Associated Membrane Protein 1/metabolism ; Lysosomes/metabolism ; Lysosomes/pathology ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Microfilament Proteins/genetics ; Microfilament Proteins/metabolism ; Multivesicular Bodies/metabolism ; Muscle Proteins/genetics ; Muscle Proteins/metabolism ; Myocytes, Smooth Muscle/metabolism ; Osteopontin/genetics ; Osteopontin/metabolism ; Real-Time Polymerase Chain Reaction ; Transient Receptor Potential Channels/genetics ; Transient Receptor Potential Channels/metabolism ; Vascular Calcification/metabolism
Chemical Substances	Core Binding Factor Alpha 1 Subunit ; Lysosomal-Associated Membrane Protein 1 ; Mcoln1 protein, mouse ; Microfilament Proteins ; Muscle Proteins ; Runx2 protein, mouse ; Transient Receptor Potential Channels ; transgelin ; Osteopontin (106441-73-0)
Language	English
Publishing date	2020-03-03
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms21051713
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