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Article ; Online: ARID1A loss is associated with increased NRF2 signaling in human head and neck squamous cell carcinomas.

Nguyen, Vinh / Schrank, Travis P / Major, Michael B / Weissman, Bernard E

2024 Volume 19, Issue 2, Page(s) e0297741

Abstract: Prior to the next generation sequencing and characterization of the tumor genome landscape, mutations in the SWI/SNF chromatin remodeling complex and the KEAP1-NRF2 signaling pathway were underappreciated. While these two classes of mutations appeared to ...

Abstract	Prior to the next generation sequencing and characterization of the tumor genome landscape, mutations in the SWI/SNF chromatin remodeling complex and the KEAP1-NRF2 signaling pathway were underappreciated. While these two classes of mutations appeared to independently contribute to tumor development, recent reports have demonstrated a mechanistic link between these two regulatory mechanisms in specific cancer types and cell models. In this work, we expand upon these data by exploring the relationship between mutations in BAF and PBAF subunits of the SWI/SNF complex and activation of NRF2 signal transduction across many cancer types. ARID1A/B mutations were strongly associated with NRF2 transcriptional activity in head and neck squamous carcinomas (HNSC). Many additional tumor types showed significant association between NRF2 signaling and mutation of specific components of the SWI/SNF complex. Different effects of BAF and PBAF mutations on the polarity of NRF2 signaling were observed. Overall, our results support a context-dependent functional link between SWI/SNF and NRF2 mutations across human cancers and implicate ARID1A inactivation in HPV-negative HNSC in promoting tumor progression and survival through activation of the KEAP1-NRF2 signaling pathway. The tumor-specific effects of these mutations open a new area of study for how mutations in the KEAP1-NRF2 pathway and the SWI/SNF complex contribute to cancer.
MeSH term(s)	Humans ; DNA-Binding Proteins/genetics ; DNA-Binding Proteins/metabolism ; Head and Neck Neoplasms/genetics ; Kelch-Like ECH-Associated Protein 1/genetics ; Kelch-Like ECH-Associated Protein 1/metabolism ; Mutation ; NF-E2-Related Factor 2/genetics ; NF-E2-Related Factor 2/metabolism ; Nuclear Proteins/genetics ; Nuclear Proteins/metabolism ; Signal Transduction/genetics ; Squamous Cell Carcinoma of Head and Neck/genetics ; Transcription Factors/genetics ; Transcription Factors/metabolism
Chemical Substances	ARID1A protein, human ; DNA-Binding Proteins ; Kelch-Like ECH-Associated Protein 1 ; NF-E2-Related Factor 2 ; Nuclear Proteins ; Transcription Factors ; NFE2L2 protein, human
Language	English
Publishing date	2024-02-15
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.0297741
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: NRF2 Activation in Trp53;p16-deficient Mice Drives Oral Squamous Cell Carcinoma.

Hamad, Samera H / Sellers, Rani S / Wamsley, Nathan / Zolkind, Paul / Schrank, Travis P / Major, Michael B / Weissman, Bernard E

Cancer research communications

2024 Volume 4, Issue 2, Page(s) 487–495

Abstract: Aberrant activation of the NRF2/NFE2L2 transcription factor commonly occurs in head and neck squamous cell carcinomas (HNSCC). Mouse model studies have shown that NRF2 activation alone does not result in cancer. When combined with classic oncogenes and ... ...

Abstract	Aberrant activation of the NRF2/NFE2L2 transcription factor commonly occurs in head and neck squamous cell carcinomas (HNSCC). Mouse model studies have shown that NRF2 activation alone does not result in cancer. When combined with classic oncogenes and at the right dose, NRF2 activation promotes tumor initiation and progression. Here we deleted the tumor suppressor genes p16INK4A and p53 (referred to as CP mice), which are commonly lost in human HNSCC, in the presence of a constitutively active NRF2E79Q mutant (CPN mice). NRF2E79Q expression in CPN mice resulted in squamous cell hyperplasia or dysplasia with hyperkeratosis in the esophagus, oropharynx, and forestomach. In addition, CPN mice displayed oral cavity squamous cell carcinoma (OSCC); CP mice bearing wild-type NRF2 expression did not develop oral cavity hyperplasia, dysplasia or OSCC. In both CP and CPN mice, we also observed predominantly abdominal sarcomas and carcinomas. Our data show that in the context of p53 and p16 tumor suppressor loss, NRF2 activation serves oncogenic functions to drive OSCC. CPN mice represent a new model for OSCC that closely reflects the genetics of human HNSCC. Significance: Human squamous cancers frequently show constitutive NRF2 activation, associated with poorer outcomes and resistance to multiple therapies. Here, we report the first activated NRF2-driven and human-relevant mouse model of squamous cell carcinoma that develops in the background of p16 and p53 loss. The availability of this model will lead to a clearer understanding of how NRF2 contributes to the initiation, progression, and therapeutic response of OSCC.
MeSH term(s)	Animals ; Humans ; Mice ; Carcinoma, Squamous Cell/genetics ; Disease Models, Animal ; Head and Neck Neoplasms/genetics ; Hyperplasia/genetics ; Mouth Neoplasms/genetics ; NF-E2-Related Factor 2/genetics ; Squamous Cell Carcinoma of Head and Neck/genetics ; Tumor Suppressor Protein p53/genetics ; Cyclin-Dependent Kinase Inhibitor p16/metabolism
Chemical Substances	NF-E2-Related Factor 2 ; Tumor Suppressor Protein p53 ; Cyclin-Dependent Kinase Inhibitor p16 ; Trp53 protein, mouse ; Nfe2l2 protein, mouse
Language	English
Publishing date	2024-02-08
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ISSN	2767-9764
ISSN (online)	2767-9764
DOI	10.1158/2767-9764.CRC-23-0386
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Article ; Online: Illuminating function of the understudied druggable kinome.

Gomez, Shawn M / Axtman, Alison D / Willson, Timothy M / Major, Michael B / Townsend, Reid R / Sorger, Peter K / Johnson, Gary L

Drug discovery today

2024 Volume 29, Issue 3, Page(s) 103881

Abstract: The human kinome, with more than 500 proteins, is crucial for cell signaling and disease. Yet, about one-third of kinases lack in-depth study. The Data and Resource Generating Center for Understudied Kinases has developed multiple resources to address ... ...

Abstract	The human kinome, with more than 500 proteins, is crucial for cell signaling and disease. Yet, about one-third of kinases lack in-depth study. The Data and Resource Generating Center for Understudied Kinases has developed multiple resources to address this challenge including creation of a heavy amino acid peptide library for parallel reaction monitoring and quantitation of protein kinase expression, use of understudied kinases tagged with a miniTurbo-biotin ligase to determine interaction networks by proximity-dependent protein biotinylation, NanoBRET probe development for screening chemical tool target specificity in live cells, characterization of small molecule chemical tools inhibiting understudied kinases, and computational tools for defining kinome architecture. These resources are available through the Dark Kinase Knowledgebase, supporting further research into these understudied protein kinases.
MeSH term(s)	Humans ; Protein Kinases/metabolism ; Proteins ; Proteomics
Chemical Substances	Protein Kinases (EC 2.7.-) ; Proteins
Language	English
Publishing date	2024-01-11
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	1324988-5
ISSN	1878-5832 ; 1359-6446
ISSN (online)	1878-5832
ISSN	1359-6446
DOI	10.1016/j.drudis.2024.103881
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Article: A basally active cGAS-STING pathway limits SARS-CoV-2 replication in a subset of ACE2 positive airway cell models.

Puray-Chavez, Maritza / LaPak, Kyle M / Jasuja, Ria / Pan, Jiehong / Xu, Jian / Eschbach, Jenna E / Mohammed, Shawn / Lawson, Dana Q / Wang, Qibo / Brody, Steven L / Major, Michael B / Goldfarb, Dennis / Kutluay, Sebla B

bioRxiv : the preprint server for biology

2024

Abstract: Host factors that define the cellular tropism of SARS-CoV-2 beyond the cognate ACE2 receptor are poorly defined. From a screen of human airway derived cell lines that express varying levels of ACE2/TMPRSS2, we found a subset that express comparably high ... ...

Abstract	Host factors that define the cellular tropism of SARS-CoV-2 beyond the cognate ACE2 receptor are poorly defined. From a screen of human airway derived cell lines that express varying levels of ACE2/TMPRSS2, we found a subset that express comparably high endogenous levels of ACE2 but surprisingly did not support SARS-CoV-2 replication. Here we report that this resistance is mediated by a basally active cGAS-STING pathway culminating in interferon (IFN)-mediated restriction of SARS-CoV-2 replication at a post-entry step. Pharmacological inhibition of JAK1/2, depletion of the IFN-α receptor and cGAS-STING pathway effectors substantially increased SARS-CoV-2 replication in these cell models. While depletion of cGAS or STING was sufficient to reduce the preexisting levels of IFN-stimulated genes (ISGs), SARS-CoV-2 infection in STING knockout cells independently induced ISG expression. Remarkably, SARS-CoV-2-induced ISG expression in STING knockout cell as well as in primary human airway cultures was limited to uninfected bystander cells, demonstrating efficient antagonism of the type I/III IFN-pathway, but not viral sensing or IFN production, in productively infected cells. Of note, SARS-CoV-2-infected primary human airway cells also displayed markedly lower levels of STING expression, raising the possibility that SARS-CoV-2 can target STING expression or preferentially infect cells that express low levels of STING. Finally, ectopic ACE2 overexpression overcame the IFN-mediated blocks, suggesting the ability of SARS-CoV-2 to overcome these possibly saturable blocks to infection. Our study highlights that in addition to viral receptors, basal activation of the cGAS-STING pathway and innate immune defenses may contribute to defining SARS-CoV-2 cellular tropism.
Language	English
Publishing date	2024-01-08
Publishing country	United States
Document type	Preprint
DOI	10.1101/2024.01.07.574522
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Article ; Online: A basally active cGAS-STING pathway limits SARS-CoV-2 replication in a subset of ACE2 positive airway cell models

Puray-Chavez, Maritza / LaPak, Kyle M. / Jasuja, Ria / Pan, Jiehong / Xu, Jian / Eschbach, Jenna E. / Mohammed, Shawn / Lawson, Dana Q. / Wang, Qibo / Brody, Steven L. / Major, Michael B. / Goldfarb, Dennis / Kutluay, Sebla B.

bioRxiv

Abstract	Host factors that define the cellular tropism of SARS-CoV-2 beyond the cognate ACE2 receptor are poorly defined. From a screen of human airway derived cell lines that express varying levels of ACE2/TMPRSS2, we found a subset that express comparably high endogenous levels of ACE2 but surprisingly did not support SARS-CoV-2 replication. Here we report that this resistance is mediated by a basally active cGAS-STING pathway culminating in interferon (IFN)-mediated restriction of SARS-CoV-2 replication at a post-entry step. Pharmacological inhibition of JAK1/2, depletion of the IFN-alpha; receptor and cGAS-STING pathway effectors substantially increased SARS-CoV-2 replication in these cell models. While depletion of cGAS or STING was sufficient to reduce the preexisting levels of IFN-stimulated genes (ISGs), SARS-CoV-2 infection in STING knockout cells independently induced ISG expression. Remarkably, SARS-CoV-2-induced ISG expression in STING knockout cell as well as in primary human airway cultures was limited to uninfected bystander cells, demonstrating efficient antagonism of the type I/III IFN-pathway, but not viral sensing or IFN production, in productively infected cells. Of note, SARS-CoV-2-infected primary human airway cells also displayed markedly lower levels of STING expression, raising the possibility that SARS-CoV-2 can target STING expression or preferentially infect cells that express low levels of STING. Finally, ectopic ACE2 overexpression overcame the IFN-mediated blocks, suggesting the ability of SARS-CoV-2 to overcome these possibly saturable blocks to infection. Our study highlights that in addition to viral receptors, basal activation of the cGAS-STING pathway and innate immune defenses may contribute to defining SARS-CoV-2 cellular tropism.
Keywords	covid19
Language	English
Publishing date	2024-01-08
Publisher	Cold Spring Harbor Laboratory
Document type	Article ; Online
DOI	10.1101/2024.01.07.574522
Database	COVID19

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Article ; Online: Positive Cooperativity in Substrate Binding by Human Thymidylate Synthase.

Bonin, Jeffrey P / Sapienza, Paul J / Wilkerson, Emily / Goldfarb, Dennis / Wang, Li / Herring, Laura / Chen, Xian / Major, Michael B / Lee, Andrew L

Biophysical journal

2021 Volume 120, Issue 18, Page(s) 4137

Language	English
Publishing date	2021-08-24
Publishing country	United States
Document type	Published Erratum
ZDB-ID	218078-9
ISSN	1542-0086 ; 0006-3495
ISSN (online)	1542-0086
ISSN	0006-3495
DOI	10.1016/j.bpj.2021.08.023
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Zs.A 235: 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)
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Article ; Online: MSAcquisitionSimulator: data-dependent acquisition simulator for LC-MS shotgun proteomics.

Goldfarb, Dennis / Wang, Wei / Major, Michael B

Bioinformatics (Oxford, England)

2016 Volume 32, Issue 8, Page(s) 1269–1271

Abstract: Unlabelled: Data-dependent acquisition (DDA) is the most common method used to control the acquisition process of shotgun proteomics experiments. While novel DDA approaches have been proposed, their evaluation is made difficult by the need of ... ...

Abstract	Unlabelled: Data-dependent acquisition (DDA) is the most common method used to control the acquisition process of shotgun proteomics experiments. While novel DDA approaches have been proposed, their evaluation is made difficult by the need of programmatic control of a mass spectrometer. An alternative is in silico analysis, for which suitable software has been unavailable. To meet this need, we have developed MSAcquisitionSimulator-a collection of C ++ programs for simulating ground truth LC-MS data and the subsequent application of custom DDA algorithms. It provides an opportunity for researchers to test, refine and evaluate novel DDA algorithms prior to implementation on a mass spectrometer. Availability and implementation: The software is freely available from its Github repository http://www.github.com/DennisGoldfarb/MSAcquisitionSimulator/ which contains further documentation and usage instructions. Contact: weiwang@cs.ucla.edu or ben_major@med.unc.edu Supplementary information: Supplementary data are available at Bioinformatics online.
MeSH term(s)	Algorithms ; Chromatography, Liquid/methods ; Humans ; Mass Spectrometry/methods ; Proteomics/methods ; Software
Language	English
Publishing date	2016-04-15
Publishing country	England
Document type	Journal Article
ZDB-ID	1422668-6
ISSN	1367-4811 ; 1367-4803
ISSN (online)	1367-4811
ISSN	1367-4803
DOI	10.1093/bioinformatics/btv745
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Article: MSAcquisitionSimulator: data-dependent acquisition simulator for LC-MS shotgun proteomics

Goldfarb, Dennis / Wang, Wei / Major, Michael B

Bioinformatics. 2016 Apr. 15, v. 32, no. 8

2016

Abstract: Summary: Data-dependent acquisition (DDA) is the most common method used to control the acquisition process of shotgun proteomics experiments. While novel DDA approaches have been proposed, their evaluation is made difficult by the need of programmatic ... ...

Abstract	Summary: Data-dependent acquisition (DDA) is the most common method used to control the acquisition process of shotgun proteomics experiments. While novel DDA approaches have been proposed, their evaluation is made difficult by the need of programmatic control of a mass spectrometer. An alternative is in silico analysis, for which suitable software has been unavailable. To meet this need, we have developed MSAcquisitionSimulator—a collection of C ++ programs for simulating ground truth LC-MS data and the subsequent application of custom DDA algorithms. It provides an opportunity for researchers to test, refine and evaluate novel DDA algorithms prior to implementation on a mass spectrometer. Availability and implementation: The software is freely available from its Github repository http://www.github.com/DennisGoldfarb/MSAcquisitionSimulator/ which contains further documentation and usage instructions. Contact: weiwang@cs.ucla.edu or ben_major@med.unc.edu Supplementary information: Supplementary data are available at Bioinformatics online.
Keywords	algorithms ; bioinformatics ; computer software ; liquid chromatography ; mass spectrometry ; proteomics ; spectrometers
Language	English
Dates of publication	2016-0415
Size	p. 1269-1271.
Publishing place	Oxford University Press
Document type	Article
ZDB-ID	1468345-3
ISSN	1460-2059 ; 1367-4811 ; 1367-4803
ISSN (online)	1460-2059 ; 1367-4811
ISSN	1367-4803
DOI	10.1093/bioinformatics/btv745
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: NRF2 Activation in Cancer: From DNA to Protein.

Cloer, Erica W / Goldfarb, Dennis / Schrank, Travis P / Weissman, Bernard E / Major, Michael B

Cancer research

2019 Volume 79, Issue 5, Page(s) 889–898

Abstract: The Cancer Genome Atlas catalogued alterations in the Kelch-like ECH-associated protein 1 and nuclear factor erythroid 2-related factor 2 (NRF2) signaling pathway in 6.3% of patient samples across 226 studies, with significant enrichment in lung and ... ...

Abstract	The Cancer Genome Atlas catalogued alterations in the Kelch-like ECH-associated protein 1 and nuclear factor erythroid 2-related factor 2 (NRF2) signaling pathway in 6.3% of patient samples across 226 studies, with significant enrichment in lung and upper airway cancers. These alterations constitutively activate NRF2-dependent gene transcription to promote many of the cancer hallmarks, including cellular resistance to oxidative stress, xenobiotic efflux, proliferation, and metabolic reprogramming. Almost universally, NRF2 activity strongly associates with poor patient prognosis and chemo- and radioresistance. Yet to date, FDA-approved drugs targeting NRF2 activity in cancer have not been realized. Here, we review various mechanisms that contribute to NRF2 activation in cancer, organized around the central dogma of molecular biology (i) at the DNA level with genomic and epigenetic alterations, (ii) at the RNA level including differential mRNA splicing and stability, and (iii) at the protein level comprising altered posttranslational modifications and protein-protein interactions. Ultimately, defining and understanding the mechanisms responsible for NRF2 activation in cancer may lead to novel targets for therapeutic intervention.
MeSH term(s)	Animals ; DNA/genetics ; DNA/metabolism ; Epigenesis, Genetic ; Humans ; NF-E2-Related Factor 2/genetics ; NF-E2-Related Factor 2/metabolism ; RNA, Messenger/genetics ; RNA, Messenger/metabolism
Chemical Substances	NF-E2-Related Factor 2 ; RNA, Messenger ; DNA (9007-49-2)
Language	English
Publishing date	2019-02-13
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1432-1
ISSN	1538-7445 ; 0008-5472
ISSN (online)	1538-7445
ISSN	0008-5472
DOI	10.1158/0008-5472.CAN-18-2723
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Article ; Online: Protein proximity networks and functional evaluation of the casein kinase 1 gamma family reveal unique roles for CK1γ3 in WNT signaling.

Agajanian, Megan J / Potjewyd, Frances M / Bowman, Brittany M / Solomon, Smaranda / LaPak, Kyle M / Bhatt, Dhaval P / Smith, Jeffery L / Goldfarb, Dennis / Axtman, Alison D / Major, Michael B

The Journal of biological chemistry

2022 Volume 298, Issue 6, Page(s) 101986

Abstract: Aberrant activation or suppression of WNT/β-catenin signaling contributes to cancer initiation and progression, neurodegeneration, and bone disease. However, despite great need and more than 40 years of research, targeted therapies for the WNT pathway ... ...

Abstract	Aberrant activation or suppression of WNT/β-catenin signaling contributes to cancer initiation and progression, neurodegeneration, and bone disease. However, despite great need and more than 40 years of research, targeted therapies for the WNT pathway have yet to be fully realized. Kinases are considered exceptionally druggable and occupy key nodes within the WNT signaling network, but several pathway-relevant kinases remain understudied and "dark." Here, we studied the function of the casein kinase 1γ (CSNK1γ) subfamily of human kinases and their roles in WNT signaling. miniTurbo-based proximity biotinylation and mass spectrometry analysis of CSNK1γ1, CSNK1γ2, and CSNK1γ3 revealed numerous components of the β-catenin-dependent and β-catenin-independent WNT pathways. In gain-of-function experiments, we found that CSNK1γ3 but not CSNK1γ1 or CSNK1γ2 activated β-catenin-dependent WNT signaling, with minimal effect on other signaling pathways. We also show that within the family, CSNK1γ3 expression uniquely induced low-density lipoprotein receptor-related protein 6 phosphorylation, which mediates downstream WNT signaling transduction. Conversely, siRNA-mediated silencing of CSNK1γ3 alone had no impact on WNT signaling, though cosilencing of all three family members decreased WNT pathway activity. Finally, we characterized two moderately selective and potent small-molecule inhibitors of the CSNK1γ family. We show that these inhibitors and a CSNK1γ3 kinase-dead mutant suppressed but did not eliminate WNT-driven low-density lipoprotein receptor-related protein 6 phosphorylation and β-catenin stabilization. Our data suggest that while CSNK1γ3 expression uniquely drives pathway activity, potential functional redundancy within the family necessitates loss of all three family members to suppress the WNT signaling pathway.
MeSH term(s)	Casein Kinase I/genetics ; Casein Kinase I/metabolism ; Humans ; Low Density Lipoprotein Receptor-Related Protein-6/genetics ; Low Density Lipoprotein Receptor-Related Protein-6/metabolism ; Phosphorylation ; Wnt Proteins/metabolism ; Wnt Signaling Pathway ; beta Catenin/genetics ; beta Catenin/metabolism
Chemical Substances	Low Density Lipoprotein Receptor-Related Protein-6 ; Wnt Proteins ; beta Catenin ; Casein Kinase I (EC 2.7.11.1)
Language	English
Publishing date	2022-04-27
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2997-x
ISSN	1083-351X ; 0021-9258
ISSN (online)	1083-351X
ISSN	0021-9258
DOI	10.1016/j.jbc.2022.101986
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