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Article: Assess Alzheimer's Disease via Plasma Extracellular Vesicle-derived mRNA.

Phu Pham, Le Hoang / Chang, Ching-Fang / Tuchez, Katherine / Chen, Yuchao

medRxiv : the preprint server for health sciences

2023

Abstract: Alzheimer's disease (AD), the most prevalent neurodegenerative disorder globally, has emerged as a significant health concern, particularly due to the increasing aging population. Recently, it has been revealed that extracellular vesicles (EVs) ... ...

Abstract	Alzheimer's disease (AD), the most prevalent neurodegenerative disorder globally, has emerged as a significant health concern, particularly due to the increasing aging population. Recently, it has been revealed that extracellular vesicles (EVs) originating from neurons play a critical role in AD pathogenesis and progression. These neuronal EVs can cross the blood-brain barrier and enter peripheral circulation, offering a less invasive means for assessing blood-based AD biomarkers. In this study, we analyzed plasma EV-derived messenger RNA (mRNA) from 82 subjects, including individuals with AD, mild cognitive impairment (MCI), and healthy controls, using next-generation sequencing (NGS) to profile their gene expression for functional enrichment and pathway analysis. Based on the differentially expressed genes identified in both MCI and AD groups, we established a diagnostic model by implementing a machine learning classifier. The refined model demonstrated an average diagnostic accuracy over 98% and showed a strong correlation with different AD stages, suggesting the potential of plasma EV-derived mRNA as a promising non-invasive biomarker for early detection and ongoing monitoring of AD.
Language	English
Publishing date	2023-12-26
Publishing country	United States
Document type	Preprint
DOI	10.1101/2023.12.26.23299985
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Article: Lamotrigine-induced pancytopenia in bipolar disorder.

Chang, Ching-Fang / Chung, Kuo-Hsuan

Journal of the Formosan Medical Association = Taiwan yi zhi

2018 Volume 117, Issue 12, Page(s) 1128–1129

MeSH term(s)	Antipsychotic Agents/adverse effects ; Antipsychotic Agents/therapeutic use ; Bipolar Disorder/drug therapy ; Female ; Humans ; Lamotrigine/adverse effects ; Lamotrigine/therapeutic use ; Middle Aged ; Pancytopenia/chemically induced ; Pancytopenia/diagnosis
Chemical Substances	Antipsychotic Agents ; Lamotrigine (U3H27498KS)
Language	English
Publishing date	2018-07-20
Publishing country	Singapore
Document type	Case Reports ; Letter
ZDB-ID	2096659-3
ISSN	1876-0821 ; 0929-6646
ISSN (online)	1876-0821
ISSN	0929-6646
DOI	10.1016/j.jfma.2018.07.004
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Article ; Online: Alcalase Potato Protein Hydrolysate-PPH902 Enhances Myogenic Differentiation and Enhances Skeletal Muscle Protein Synthesis under High Glucose Condition in C2C12 Cells.

Chen, Yi-Ju / Chang, Ching-Fang / Angayarkanni, Jayaraman / Lin, Wan-Teng

Molecules (Basel, Switzerland)

2021 Volume 26, Issue 21

Abstract: Sarcopenia is an aging associated disorder involving skeletal muscle atrophy and a reduction in muscle strength, and there are no pharmaceutical interventions available thus far. Moreover, conditions such as hyperglycaemia are known to further intensify ... ...

Abstract	Sarcopenia is an aging associated disorder involving skeletal muscle atrophy and a reduction in muscle strength, and there are no pharmaceutical interventions available thus far. Moreover, conditions such as hyperglycaemia are known to further intensify muscle degradation. Therefore, novel strategies to attenuate skeletal muscle loss are essential to enhance muscle function and thereby improve the quality of life in diabetic individuals. In this study, we have investigated the efficiency of a potato peptide hydrolysate PPH902 for its cytoprotective effects in skeletal muscle cells. PPH902 treatment in C2C12 cells showed the dose-dependent activation of the Akt/mTOR signalling pathway that is involved in skeletal myogenesis. According to Western blotting analysis, PPH902 induced the phosphorylation of Akt, mTOR proteins and induced the myogenic differentiation of C2C12 myoblasts in a differentiation medium. The phosphorylation myogenic transcription factor Foxo3A was also found to be increased in the cells treated with PPH902. In addition, treatment with PPH902 ameliorated the high glucose induced reduction in cell viability in a dose-dependent manner. Moreover, the number of myotubes in a differentiation medium reduced upon high glucose challenge, but treatment with PPH902 increased the number of differentiated myotubes. Further, the phosphorylations of AMPK and mitochondrial-related transcription factors such as PGC-1α were suppressed upon high glucose challenge but PPH902 treatment restored the protein levels. We demonstrate, for the first time, that a specific potato peptide has a therapeutic effect against sarcopenia. In addition, PPH902 improved the myogenic differentiation and their mitochondrial biogenesis and further improved myogenic protein and inhibited muscle protein degradation in C2C12 cells challenged under a high glucose condition.
MeSH term(s)	Animals ; Cell Differentiation/drug effects ; Cells, Cultured ; Dose-Response Relationship, Drug ; Forkhead Box Protein O3/biosynthesis ; Forkhead Box Protein O3/chemistry ; Glucose/metabolism ; Mice ; Muscle Development/drug effects ; Protein Hydrolysates
Chemical Substances	Forkhead Box Protein O3 ; FoxO3 protein, mouse ; Protein Hydrolysates ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	2021-10-30
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	1413402-0
ISSN	1420-3049 ; 1431-5165 ; 1420-3049
ISSN (online)	1420-3049
ISSN	1431-5165 ; 1420-3049
DOI	10.3390/molecules26216577
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Article: Centriolar Protein C2cd3 Is Required for Craniofacial Development.

Chang, Ching-Fang / Brown, Kari M / Yang, Yanfen / Brugmann, Samantha A

Frontiers in cell and developmental biology

2021 Volume 9, Page(s) 647391

Abstract: The primary cilium is a ubiquitous, microtubule-based cellular organelle. Primary cilia dysfunction results in a group of disorders termed ciliopathies. C2 domain containing 3 centriole elongation regulator (C2cd3), encodes a centriolar protein essential ...

Abstract	The primary cilium is a ubiquitous, microtubule-based cellular organelle. Primary cilia dysfunction results in a group of disorders termed ciliopathies. C2 domain containing 3 centriole elongation regulator (C2cd3), encodes a centriolar protein essential for ciliogenesis. Mutations in human C2CD3 are associated with the human ciliopathy Oral-Facial-Digital syndrome type 14 (OFD14). In order to better understand the etiology of ciliopathies including OFD14, we generated numerous murine models targeting C2cd3. Initial analysis revealed several tissue-specific isoforms of C2cd3, and while the loss of C2cd3 has previously been reported to result in exencephaly, tight mesencephalic flexure, pericardial edema, abnormal heart looping and a twisted body axis, further analysis revealed that genetic background may also contribute to phenotypic variation. Additional analyses of a conditional allelic series targeting C-terminal PKC-C2 domains or the N-terminal C2CD3N-C2 domain of C2cd3 revealed a variable degree of phenotypic severity, suggesting that while the N-terminal C2CD3N-C2 domain was critical for early embryonic development as a whole, there was also a craniofacial specific role for the C2CD3N-C2 domains. Together, through generation of novel models and evaluation of C2cd3 expression, these data provide valuable insight into mechanisms of pathology for craniofacial ciliopathies that can be further explored in the future.
Language	English
Publishing date	2021-06-15
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2737824-X
ISSN	2296-634X
ISSN	2296-634X
DOI	10.3389/fcell.2021.647391
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Article ; Online: Decapeptide from Potato Hydrolysate Induces Myogenic Differentiation and Ameliorates High Glucose-Associated Modulations in Protein Synthesis and Mitochondrial Biogenesis in C2C12 Cells.

Chen, Yi-Ju / Baskaran, Rathinasamy / Chang, Ching Fang / Mohammedsaleh, Zuhair M / Lin, Wan-Teng

Biomolecules

2022 Volume 12, Issue 4

Abstract: Sarcopenia is characterized as an age-related loss of muscle mass that results in negative health consequences such as decreased strength, insulin resistance, slowed metabolism, increased body fat mass, and a substantially diminished quality of life. ... ...

Abstract	Sarcopenia is characterized as an age-related loss of muscle mass that results in negative health consequences such as decreased strength, insulin resistance, slowed metabolism, increased body fat mass, and a substantially diminished quality of life. Additionally, conditions such as high blood sugar are known to further exacerbate muscle degeneration. Skeletal muscle development and regeneration following injury or disease are based on myoblast differentiation. Bioactive peptides are biologically active peptides found in foods that could have pharmacological functions. The aim of this paper was to investigate the effect of decapeptide DI-10 from the potato alcalase hydrolysate on myoblast differentiation, muscle protein synthesis, and mitochondrial biogenesis in vitro. The treatment of C2C12 myoblasts with DI-10 (10 µg/mL) did not induce cell death. DI-10 treatment in C2C12 myoblast cells accelerates the phosphorylation of promyogenic kinases such as ERK, Akt and mTOR proteins in a dose-dependent manner. DI-10 improves myotubes differentiation and upregulates the expression of myosin heavy chain (MyHC) protein in myoblast cells under differentiation medium with high glucose. DI-10 effectively increased the phosphorylation of promyogenic kinases Akt, mTOR, and mitochondrial-related transcription factors AMPK and PGC1α expression under hyperglycemic conditions. Further, decapeptide DI-10 decreased the expression of Murf1 and MAFbx proteins, which are involved in protein degradation and muscle atrophy. Our reports support that decapeptide DI-10 could be potentially used as a therapeutic candidate for preventing muscle degeneration in sarcopenia.
MeSH term(s)	Cell Differentiation ; Glucose/metabolism ; Glucose/pharmacology ; Humans ; Muscle Development ; Muscle, Skeletal/metabolism ; Organelle Biogenesis ; Proto-Oncogene Proteins c-akt/metabolism ; Quality of Life ; Sarcopenia ; Solanum tuberosum/metabolism ; TOR Serine-Threonine Kinases/metabolism
Chemical Substances	Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; TOR Serine-Threonine Kinases (EC 2.7.11.1) ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	2022-04-11
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2701262-1
ISSN	2218-273X ; 2218-273X
ISSN (online)	2218-273X
ISSN	2218-273X
DOI	10.3390/biom12040565
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Article ; Online: Pharmacological intervention of the FGF-PTH axis as a potential therapeutic for craniofacial ciliopathies.

Bonatto Paese, Christian Louis / Chang, Ching-Fang / Kristeková, Daniela / Brugmann, Samantha A

Disease models & mechanisms

2022 Volume 15, Issue 8

Abstract: Ciliopathies represent a disease class characterized by a broad range of phenotypes including polycystic kidneys and skeletal anomalies. Ciliopathic skeletal phenotypes are among the most common and most difficult to treat due to a poor understanding of ... ...

Abstract	Ciliopathies represent a disease class characterized by a broad range of phenotypes including polycystic kidneys and skeletal anomalies. Ciliopathic skeletal phenotypes are among the most common and most difficult to treat due to a poor understanding of the pathological mechanisms leading to disease. Using an avian model (talpid2) for a human ciliopathy with both kidney and skeletal anomalies (orofaciodigital syndrome 14), we identified disruptions in the FGF23-PTH axis that resulted in reduced calcium uptake in the developing mandible and subsequent micrognathia. Although pharmacological intervention with the U.S. Food and Drug Administration (FDA)-approved pan-FGFR inhibitor AZD4547 alone rescued expression of the FGF target SPRY2, it did not significantly rescue micrognathia. In contrast, treatment with a cocktail of AZD4547 and teriparatide acetate, a PTH agonist and FDA-approved treatment for osteoporosis, resulted in molecular, cellular and phenotypic rescue of ciliopathic micrognathia in talpid2 mutants. Together, these data provide novel insight into pathological molecular mechanisms associated with ciliopathic skeletal phenotypes and a potential therapeutic strategy for a pleiotropic disease class with limited to no treatment options.
MeSH term(s)	Cilia/metabolism ; Ciliopathies/drug therapy ; Ciliopathies/genetics ; Ciliopathies/metabolism ; Humans ; Intracellular Signaling Peptides and Proteins/metabolism ; Membrane Proteins/metabolism ; Micrognathism/metabolism ; Micrognathism/pathology ; Phenotype ; Proteins/metabolism
Chemical Substances	Intracellular Signaling Peptides and Proteins ; Membrane Proteins ; Proteins ; SPRY2 protein, human
Language	English
Publishing date	2022-08-16
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2451104-3
ISSN	1754-8411 ; 1754-8403
ISSN (online)	1754-8411
ISSN	1754-8403
DOI	10.1242/dmm.049611
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Article ; Online: Brown adipose tissue CoQ deficiency activates the integrated stress response and FGF21-dependent mitohormesis.

Chang, Ching-Fang / Gunawan, Amanda L / Liparulo, Irene / Zushin, Peter-James H / Vitangcol, Kaitlyn / Timblin, Greg A / Saijo, Kaoru / Wang, Biao / Parlakgül, Güneş / Arruda, Ana Paula / Stahl, Andreas

The EMBO journal

2024 Volume 43, Issue 2, Page(s) 168–195

Abstract: Coenzyme Q (CoQ) is essential for mitochondrial respiration and required for thermogenic activity in brown adipose tissues (BAT). CoQ deficiency leads to a wide range of pathological manifestations, but mechanistic consequences of CoQ deficiency in ... ...

Abstract	Coenzyme Q (CoQ) is essential for mitochondrial respiration and required for thermogenic activity in brown adipose tissues (BAT). CoQ deficiency leads to a wide range of pathological manifestations, but mechanistic consequences of CoQ deficiency in specific tissues, such as BAT, remain poorly understood. Here, we show that pharmacological or genetic CoQ deficiency in BAT leads to stress signals causing accumulation of cytosolic mitochondrial RNAs and activation of the eIF2α kinase PKR, resulting in activation of the integrated stress response (ISR) with suppression of UCP1 but induction of FGF21 expression. Strikingly, despite diminished UCP1 levels, BAT CoQ deficiency displays increased whole-body metabolic rates at room temperature and thermoneutrality resulting in decreased weight gain on high-fat diets (HFD). In line with enhanced metabolic rates, BAT and inguinal white adipose tissue (iWAT) interorgan crosstalk caused increased browning of iWAT in BAT-specific CoQ deficient animals. This mitohormesis-like effect depends on the ATF4-FGF21 axis and BAT-secreted FGF21, revealing an unexpected role for CoQ in the modulation of whole-body energy expenditure with wide-ranging implications for primary and secondary CoQ deficiencies.
MeSH term(s)	Animals ; Mice ; Adipose Tissue, Brown/metabolism ; Ubiquinone/metabolism ; Ubiquinone/pharmacology ; Mitochondrial Diseases/metabolism ; Thermogenesis/genetics ; Mice, Inbred C57BL ; Ataxia ; Fibroblast Growth Factors ; Muscle Weakness
Chemical Substances	fibroblast growth factor 21 ; Ubiquinone (1339-63-5) ; Fibroblast Growth Factors (62031-54-3)
Language	English
Publishing date	2024-01-11
Publishing country	England
Document type	Journal Article
ZDB-ID	586044-1
ISSN	1460-2075 ; 0261-4189
ISSN (online)	1460-2075
ISSN	0261-4189
DOI	10.1038/s44318-023-00008-x
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Article: CoQ Regulates Brown Adipose Tissue Respiration and Uncoupling Protein 1 Expression.

Chang, Ching-Fang / Gunawan, Amanda L / Liparulo, Irene / Zushin, Peter-James H / Bertholet, Ambre M / Kirichok, Yuriy / Stahl, Andreas

Antioxidants (Basel, Switzerland)

2022 Volume 12, Issue 1

Abstract: Coenzyme Q (CoQ, aka ubiquinone) is a key component of the mitochondrial electron transport chain (ETC) and membrane-incorporated antioxidant. CoQ10 deficiencies encompass a heterogeneous spectrum of clinical phenotypes and can be caused by hereditary ... ...

Abstract	Coenzyme Q (CoQ, aka ubiquinone) is a key component of the mitochondrial electron transport chain (ETC) and membrane-incorporated antioxidant. CoQ10 deficiencies encompass a heterogeneous spectrum of clinical phenotypes and can be caused by hereditary mutations in the biosynthesis pathway or result from pharmacological interventions such as HMG-CoA Reductase inhibitors, and statins, which are widely used to treat hypercholesterolemia and prevent cardiovascular disease. How CoQ deficiency affects individual tissues and cell types, particularly mitochondrial-rich ones such as brown adipose tissue (BAT), has remained poorly understood. Here we show that pharmacological and genetic models of BAT CoQ deficiency show altered respiration that can only in part be explained by classical roles of CoQ in the respiration chain. Instead, we found that CoQ strongly impacts brown and beige adipocyte respiration via the regulation of uncoupling protein 1 (UCP1) expression. CoQ deficiency in BAT robustly decreases UCP1 protein levels and uncoupled respiration unexpectedly, resulting in increased inner mitochondrial membrane potential and decreased ADP/ATP ratios. Suppressed UCP1 expression was also observed in a BAT-specific in vivo model of CoQ deficiency and resulted in enhanced cold sensitivity. These findings demonstrate an as yet unappreciated role of CoQ in the transcriptional regulation of key thermogenic genes and functions.
Language	English
Publishing date	2022-12-22
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2704216-9
ISSN	2076-3921
ISSN	2076-3921
DOI	10.3390/antiox12010014
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Article ; Online: Probing Insulin Sensitivity with Metabolically Competent Human Stem Cell-Derived White Adipose Tissue Microphysiological Systems.

Qi, Lin / Zushin, Peter-James H / Chang, Ching-Fang / Lee, Yue Tung / Alba, Diana L / Koliwad, Suneil K / Stahl, Andreas

Small (Weinheim an der Bergstrasse, Germany)

2021 Volume 18, Issue 3, Page(s) e2103157

Abstract: Impaired white adipose tissue (WAT) function has been recognized as a critical early event in obesity-driven disorders, but high buoyancy, fragility, and heterogeneity of primary adipocytes have largely prevented their use in drug discovery efforts ... ...

Abstract	Impaired white adipose tissue (WAT) function has been recognized as a critical early event in obesity-driven disorders, but high buoyancy, fragility, and heterogeneity of primary adipocytes have largely prevented their use in drug discovery efforts highlighting the need for human stem cell-based approaches. Here, human stem cells are utilized to derive metabolically functional 3D adipose tissue (iADIPO) in a microphysiological system (MPS). Surprisingly, previously reported WAT differentiation approaches create insulin resistant WAT ill-suited for type-2 diabetes mellitus drug discovery. Using three independent insulin sensitivity assays, i.e., glucose and fatty acid uptake and suppression of lipolysis, as the functional readouts new differentiation conditions yielding hormonally responsive iADIPO are derived. Through concomitant optimization of an iADIPO-MPS, it is abled to obtain WAT with more unilocular and significantly larger (≈40%) lipid droplets compared to iADIPO in 2D culture, increased insulin responsiveness of glucose uptake (≈2-3 fold), fatty acid uptake (≈3-6 fold), and ≈40% suppressing of stimulated lipolysis giving a dynamic range that is competent to current in vivo and ex vivo models, allowing to identify both insulin sensitizers and desensitizers.
MeSH term(s)	Adipocytes ; Adipose Tissue ; Adipose Tissue, White ; Humans ; Insulin ; Insulin Resistance ; Stem Cells
Chemical Substances	Insulin
Language	English
Publishing date	2021-11-10
Publishing country	Germany
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2168935-0
ISSN	1613-6829 ; 1613-6810
ISSN (online)	1613-6829
ISSN	1613-6810
DOI	10.1002/smll.202103157
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Article ; Online: Ift88 regulates Hedgehog signaling, Sfrp5 expression, and β-catenin activity in post-natal growth plate.

Chang, Ching-Fang / Serra, Rosa

Journal of orthopaedic research : official publication of the Orthopaedic Research Society

2012 Volume 31, Issue 3, Page(s) 350–356

Abstract: Primary cilia are present on most cell types including chondrocytes. Dysfunction of primary cilia results in pleiotropic symptoms including skeletal dysplasia. Previously, we showed that deletion of Ift88 and subsequent depletion of primary cilia from ... ...

Abstract	Primary cilia are present on most cell types including chondrocytes. Dysfunction of primary cilia results in pleiotropic symptoms including skeletal dysplasia. Previously, we showed that deletion of Ift88 and subsequent depletion of primary cilia from chondrocytes resulted in disorganized columnar structure and early loss of growth plate. To understand underlying mechanisms whereby Ift88 regulates growth plate function, we compared gene expression profiles in normal and Ift88 deleted growth plates. Pathway analysis indicated that Hedgehog (Hh) signaling was the most affected pathway in mutant growth plate. Expression of the Wnt antagonist, Sfrp5, was also down-regulated. In addition, Sfrp5 was up-regulated by Shh in rib chondrocytes and regulation of Sfrp5 by Shh was attenuated in mutant cells. This result suggests Sfrp5 is a downstream target of Hh and that Ift88 regulates its expression. Sfrp5 is an extracellular antagonist of Wnt signaling. We observed an increase in Wnt/β-catenin signaling specifically in flat columnar cells of the growth plate in Ift88 mutant mice as measured by increased expression of Axin2 and Lef1 as well as increased nuclear localization of β-catenin. We propose that Ift88 and primary cilia regulate expression of Sfrp5 and Wnt signaling pathways in growth plate via regulation of Ihh signaling.
MeSH term(s)	Adaptor Proteins, Signal Transducing ; Animals ; Cells, Cultured ; Chondrocytes/cytology ; Chondrocytes/metabolism ; Cilia/metabolism ; Down-Regulation/genetics ; Growth Plate/cytology ; Growth Plate/metabolism ; Hedgehog Proteins/metabolism ; Intercellular Signaling Peptides and Proteins/metabolism ; Mice ; Mice, Mutant Strains ; Ribs/cytology ; Ribs/growth & development ; Ribs/physiology ; Transcriptome/physiology ; Tumor Suppressor Proteins/genetics ; Tumor Suppressor Proteins/metabolism ; Up-Regulation/genetics ; Wnt Signaling Pathway/physiology ; beta Catenin/metabolism
Chemical Substances	Adaptor Proteins, Signal Transducing ; CTNNB1 protein, mouse ; Hedgehog Proteins ; Intercellular Signaling Peptides and Proteins ; Sfrp5 protein, mouse ; Shh protein, mouse ; Tg737Rpw protein, mouse ; Tumor Suppressor Proteins ; beta Catenin
Language	English
Publishing date	2012-10-03
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	605542-4
ISSN	1554-527X ; 0736-0266
ISSN (online)	1554-527X
ISSN	0736-0266
DOI	10.1002/jor.22237
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