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Article ; Online: PP2A activation targets AML stem cells.

Verrills, Nicole M

2022 Volume 139, Issue 9, Page(s) 1267–1269

MeSH term(s)	Humans ; Leukemia, Myeloid, Acute/genetics ; Protein Phosphatase 2 ; Stem Cells
Chemical Substances	Protein Phosphatase 2 (EC 3.1.3.16)
Language	English
Publishing date	2022-03-07
Publishing country	United States
Document type	Editorial ; Comment
ZDB-ID	80069-7
ISSN	1528-0020 ; 0006-4971
ISSN (online)	1528-0020
ISSN	0006-4971
DOI	10.1182/blood.2021014677
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Article ; Online: Pharmaco-phosphoproteomic analysis of cancer-associated KIT mutations D816V and V560G.

Murray, Heather C / Miller, Kasey / Dun, Matthew D / Verrills, Nicole M

Proteomics

2024 Volume 24, Issue 9, Page(s) e2300309

Abstract: The CD117 mast/stem cell growth factor receptor tyrosine kinase (KIT) is critical for haematopoiesis, melanogenesis and stem cell maintenance. KIT is commonly activated by mutation in cancers including acute myeloid leukaemia, melanoma and ... ...

Abstract	The CD117 mast/stem cell growth factor receptor tyrosine kinase (KIT) is critical for haematopoiesis, melanogenesis and stem cell maintenance. KIT is commonly activated by mutation in cancers including acute myeloid leukaemia, melanoma and gastrointestinal stromal tumours (GISTs). The kinase and the juxtamembrane domains of KIT are mutation hotspots; with the kinase domain mutation D816V common in leukaemia and the juxtamembrane domain mutation V560G common in GISTs. Given the importance of mutant KIT signalling in cancer, we have conducted a proteomic and phosphoproteomic analysis of myeloid progenitor cells expressing D816V- and V560G-KIT mutants, using an FDCP1 isogenic cell line model. Proteomic analysis revealed increased abundance of proteases and growth signalling proteins in KIT-mutant cells compared to empty vector (EV) controls. Pathway analysis identified increased oxidative phosphorylation in D816V- and V560G-mutant KIT cells, which was targetable using the inhibitor IACS010759. Dysregulation of RNA metabolism and cytoskeleton/adhesion pathways was identified in both the proteome and phosphoproteome of KIT-mutant cells. Phosphoproteome analysis further revealed active kinases such as EGFR, ERK and PKC, which were targetable using pharmacological inhibitors. This study provides a pharmaco-phosphoproteomic profile of D816V- and V560G-mutant KIT cells, which reveals novel therapeutic strategies that may be applicable to a range of cancers.
MeSH term(s)	Proto-Oncogene Proteins c-kit/genetics ; Proto-Oncogene Proteins c-kit/metabolism ; Humans ; Proteomics/methods ; Mutation ; Cell Line, Tumor ; Neoplasms/genetics ; Neoplasms/metabolism ; Neoplasms/pathology ; Phosphoproteins/genetics ; Phosphoproteins/metabolism ; Signal Transduction/genetics ; Phosphorylation ; Proteome/genetics ; Proteome/metabolism ; Proteome/analysis
Chemical Substances	Proto-Oncogene Proteins c-kit (EC 2.7.10.1) ; KIT protein, human (EC 2.7.10.1) ; Phosphoproteins ; Proteome
Language	English
Publishing date	2024-02-09
Publishing country	Germany
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2032093-0
ISSN	1615-9861 ; 1615-9853
ISSN (online)	1615-9861
ISSN	1615-9853
DOI	10.1002/pmic.202300309
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Zs.A 5386: 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)
Zs.A 1868: 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: Proteomic and phosphoproteomic characterisation of primary mouse embryonic fibroblasts.

Chen, Yanfang / Roselli, Severine / Panicker, Nikita / Brzozowski, Joshua S / Skerrett-Byrne, David A / Murray, Heather C / Verrills, Nicole M

Proteomics

2023 Volume 24, Issue 7, Page(s) e2300267

Abstract: Fibroblasts are the most common cell type in stroma and function in the support and repair of most tissues. Mouse embryonic fibroblasts (MEFs) are amenable to isolation and rapid growth in culture. MEFs are therefore widely used as a standard model for ... ...

Abstract	Fibroblasts are the most common cell type in stroma and function in the support and repair of most tissues. Mouse embryonic fibroblasts (MEFs) are amenable to isolation and rapid growth in culture. MEFs are therefore widely used as a standard model for functional characterisation of gene knockouts, and can also be used in co-cultures, commonly to support embryonic stem cell cultures. To facilitate their use as a research tool, we have performed a comprehensive proteomic and phosphoproteomic characterisation of wild-type primary MEFs from C57BL/6 mice. EIF2/4 and MTOR signalling pathways were abundant in both the proteome and phosphoproteome, along with extracellular matrix (ECM) and cytoskeleton associated pathways. Consistent with this, kinase enrichment analysis identified activation of P38A, P90RSK, P70S6K, and MTOR. Cell surface markers and matrisome proteins were also annotated. Data are available via ProteomeXchange with identifier PXD043244. This provides a comprehensive catalogue of the wild-type MEF proteome and phosphoproteome which can be utilised by the field to guide future work.
MeSH term(s)	Animals ; Mice ; Proteome/analysis ; Proteomics ; Fibroblasts/metabolism ; Mice, Inbred C57BL ; TOR Serine-Threonine Kinases/metabolism
Chemical Substances	Proteome ; TOR Serine-Threonine Kinases (EC 2.7.11.1)
Language	English
Publishing date	2023-10-17
Publishing country	Germany
Document type	Journal Article
ZDB-ID	2032093-0
ISSN	1615-9861 ; 1615-9853
ISSN (online)	1615-9861
ISSN	1615-9853
DOI	10.1002/pmic.202300267
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Zs.A 5386: 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)
Zs.A 1868: 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: Synergistic Targeting of DNA-PK and KIT Signaling Pathways in KIT Mutant Acute Myeloid Leukemia.

Murray, Heather C / Miller, Kasey / Brzozowski, Joshua S / Kahl, Richard G S / Smith, Nathan D / Humphrey, Sean J / Dun, Matthew D / Verrills, Nicole M

Molecular & cellular proteomics : MCP

2023 Volume 22, Issue 3, Page(s) 100503

Abstract: Acute myeloid leukemia (AML) is the most common and aggressive form of acute leukemia, with a 5-year survival rate of just 24%. Over a third of all AML patients harbor activating mutations in kinases, such as the receptor tyrosine kinases FLT3 (receptor- ... ...

Abstract	Acute myeloid leukemia (AML) is the most common and aggressive form of acute leukemia, with a 5-year survival rate of just 24%. Over a third of all AML patients harbor activating mutations in kinases, such as the receptor tyrosine kinases FLT3 (receptor-type tyrosine-protein kinase FLT3) and KIT (mast/stem cell growth factor receptor kit). FLT3 and KIT mutations are associated with poor clinical outcomes and lower remission rates in response to standard-of-care chemotherapy. We have recently identified that the core kinase of the non-homologous end joining DNA repair pathway, DNA-PK (DNA-dependent protein kinase), is activated downstream of FLT3; and targeting DNA-PK sensitized FLT3-mutant AML cells to standard-of-care therapies. Herein, we investigated DNA-PK as a possible therapeutic vulnerability in KIT mutant AML, using isogenic FDC-P1 mouse myeloid progenitor cell lines transduced with oncogenic mutant KIT (V560G and D816V) or vector control. Targeted quantitative phosphoproteomic profiling identified phosphorylation of DNA-PK in the T2599/T2605/S2608/S2610 cluster in KIT mutant cells, indicative of DNA-PK activation. Accordingly, proliferation assays revealed that KIT mutant FDC-P1 cells were more sensitive to the DNA-PK inhibitors M3814 or NU7441, compared with empty vector controls. DNA-PK inhibition combined with inhibition of KIT signaling using the kinase inhibitors dasatinib or ibrutinib, or the protein phosphatase 2A activators FTY720 or AAL(S), led to synergistic cell death. Global phosphoproteomic analysis of KIT-D816V cells revealed that dasatinib and M3814 single-agent treatments inhibited extracellular signal-regulated kinase and AKT (RAC-alpha serine/threonine-protein kinase)/MTOR (serine/threonine-protein kinase mTOR) activity, with greater inhibition of both pathways when used in combination. Combined dasatinib and M3814 treatment also synergistically inhibited phosphorylation of the transcriptional regulators MYC and MYB. This study provides insight into the oncogenic pathways regulated by DNA-PK beyond its canonical role in DNA repair and demonstrates that DNA-PK is a promising therapeutic target for KIT mutant cancers.
MeSH term(s)	Animals ; Mice ; Apoptosis ; Cell Line, Tumor ; Dasatinib ; DNA ; DNA-Activated Protein Kinase/genetics ; Leukemia, Myeloid, Acute/genetics ; Leukemia, Myeloid, Acute/drug therapy ; Mutation ; Protein Kinase Inhibitors/pharmacology ; Receptor Protein-Tyrosine Kinases ; Serine ; Signal Transduction ; Threonine ; TOR Serine-Threonine Kinases ; Tyrosine
Chemical Substances	Dasatinib (RBZ1571X5H) ; DNA (9007-49-2) ; DNA-Activated Protein Kinase (EC 2.7.11.1) ; Protein Kinase Inhibitors ; Receptor Protein-Tyrosine Kinases (EC 2.7.10.1) ; Serine (452VLY9402) ; Threonine (2ZD004190S) ; TOR Serine-Threonine Kinases (EC 2.7.11.1) ; Tyrosine (42HK56048U) ; Kit protein, mouse
Language	English
Publishing date	2023-01-20
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2075924-1
ISSN	1535-9484 ; 1535-9476
ISSN (online)	1535-9484
ISSN	1535-9476
DOI	10.1016/j.mcpro.2023.100503
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Article ; Online: Phosphoproteomic analysis of the adaption of epididymal epithelial cells to corticosterone challenge.

Skerrett-Byrne, David A / Stanger, Simone J / Trigg, Natalie A / Anderson, Amanda L / Sipilä, Petra / Bernstein, Ilana R / Lord, Tessa / Schjenken, John E / Murray, Heather C / Verrills, Nicole M / Dun, Matthew D / Pang, Terence Y / Nixon, Brett

Andrology

2024

Abstract: Background: The epididymis has long been of interest owing to its role in promoting the functional maturation of the male germline. More recent evidence has also implicated the epididymis as an important sensory tissue responsible for remodeling of the ... ...

Abstract	Background: The epididymis has long been of interest owing to its role in promoting the functional maturation of the male germline. More recent evidence has also implicated the epididymis as an important sensory tissue responsible for remodeling of the sperm epigenome, both under physiological conditions and in response to diverse forms of environmental stress. Despite this knowledge, the intricacies of the molecular pathways involved in regulating the adaptation of epididymal tissue to paternal stressors remains to be fully resolved. Objective: The overall objective of this study was to investigate the direct impact of corticosterone challenge on a tractable epididymal epithelial cell line (i.e., mECap18 cells), in terms of driving adaptation of the cellular proteome and phosphoproteome signaling networks. Materials and methods: The newly developed phosphoproteomic platform EasyPhos coupled with sequencing via an Orbitrap Exploris 480 mass spectrometer, was applied to survey global changes in the mECap18 cell (phospho)proteome resulting from sub-chronic (10-day) corticosterone challenge. Results: The imposed corticosterone exposure regimen elicited relatively subtle modifications of the global mECap18 proteome (i.e., only 73 out of 4171 [∼1.8%] proteins displayed altered abundance). By contrast, ∼15% of the mECap18 phosphoproteome was substantially altered following corticosterone challenge. In silico analysis of the corresponding parent proteins revealed an activation of pathways linked to DNA damage repair and oxidative stress responses as well as a reciprocal inhibition of pathways associated with organismal death. Corticosterone challenge also induced the phosphorylation of several proteins linked to the biogenesis of microRNAs. Accordingly, orthogonal validation strategies confirmed an increase in DNA damage, which was ameliorated upon selective kinase inhibition, and an altered abundance profile of a subset of microRNAs in corticosterone-treated cells. Conclusions: Together, these data confirm that epididymal epithelial cells are reactive to corticosterone challenge, and that their response is tightly coupled to the opposing action of cellular kinases and phosphatases.
Language	English
Publishing date	2024-04-04
Publishing country	England
Document type	Journal Article
ZDB-ID	2696108-8
ISSN	2047-2927 ; 2047-2919
ISSN (online)	2047-2927
ISSN	2047-2919
DOI	10.1111/andr.13636
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Article ; Online: scTEM-seq: Single-cell analysis of transposable element methylation to link global epigenetic heterogeneity with transcriptional programs.

Hunt, Kooper V / Burnard, Sean M / Roper, Ellise A / Bond, Danielle R / Dun, Matthew D / Verrills, Nicole M / Enjeti, Anoop K / Lee, Heather J

Scientific reports

2022 Volume 12, Issue 1, Page(s) 5776

Abstract: Global changes in DNA methylation are observed in development and disease, and single-cell analyses are highlighting the heterogeneous regulation of these processes. However, technical challenges associated with single-cell analysis of DNA methylation ... ...

Abstract	Global changes in DNA methylation are observed in development and disease, and single-cell analyses are highlighting the heterogeneous regulation of these processes. However, technical challenges associated with single-cell analysis of DNA methylation limit these studies. We present single-cell transposable element methylation sequencing (scTEM-seq) for cost-effective estimation of average DNA methylation levels. By targeting high-copy SINE Alu elements, we achieve amplicon bisulphite sequencing with thousands of loci covered in each scTEM-seq library. Parallel transcriptome analysis is also performed to link global DNA methylation estimates with gene expression. We apply scTEM-seq to KG1a acute myeloid leukaemia (AML) cells, and primary AML cells. Our method reveals global DNA methylation heterogeneity induced by decitabine treatment of KG1a cells associated with altered expression of immune process genes. We also compare global DNA methylation estimates to expression of transposable elements and find a predominance of negative correlations. Finally, we observe co-ordinated upregulation of many transposable elements in a sub-set of decitabine treated cells. By linking global DNA methylation heterogeneity with transcription, scTEM-seq will refine our understanding of epigenetic regulation in cancer and beyond.
MeSH term(s)	DNA Methylation ; DNA Transposable Elements/genetics ; Decitabine/pharmacology ; Epigenesis, Genetic ; Humans ; Leukemia, Myeloid, Acute/genetics ; Single-Cell Analysis
Chemical Substances	DNA Transposable Elements ; Decitabine (776B62CQ27)
Language	English
Publishing date	2022-04-06
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-022-09765-x
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Article ; Online: The impact of a regionally based translational cancer research collaborative in Australia using the FAIT methodology.

Paul, Christine L / Verrills, Nicole M / Ackland, Stephen / Scott, Rodney / Goode, Susan / Thomas, Ann / Lukeman, Sarah / Nielsen, Sarah / Weidenhofer, Judith / Lynam, James / Fradgley, Elizabeth A / Martin, Jarad / Greer, Peter / Smith, Stephen / Griffin, Cassandra / Avery-Kiejda, Kelly A / Zdenkowski, Nick / Searles, Andrew / Ramanathan, Shanthi

BMC health services research

2024 Volume 24, Issue 1, Page(s) 320

Abstract: ... ii) conservatively leveraging $43.8 M (s.a.$20.5 M - $160.5 M) in funding and support ... from the initial $9.7 M investment; (iii) contributing to clinical practice guidelines and securing a patent ...

Abstract	Background: Translating research, achieving impact, and assessing impact are important aspirations for all research collaboratives but can prove challenging. The Hunter Cancer Research Alliance (HCRA) was funded from 2014 to 2021 to enhance capacity and productivity in cancer research in a regional centre in Australia. This study aimed to assess the impact and benefit of the HCRA to help inform future research investments of this type. Method: The Framework to Assess the Impact from Translational health research (FAIT) was selected as the preferred methodology. FAIT incorporates three validated methodologies for assessing impact: 1) Modified Payback; 2) Economic Analysis; and 3) Narrative overview and case studies. All three FAIT methods are underpinned by a Program Logic Model. Data were collected from HCRA and the University of Newcastle administrative records, directly from HCRA members, and website searches. Results: In addition to advancing knowledge and providing capacity building support to members via grants, fellowships, scholarships, training, events and targeted translation support, key impacts of HCRA-member research teams included: (i) the establishment of a regional biobank that has distributed over 13,600 samples and became largely self-sustaining; (ii) conservatively leveraging $43.8 M (s.a.$20.5 M - $160.5 M) in funding and support from the initial $9.7 M investment; (iii) contributing to clinical practice guidelines and securing a patent for identification of stem cells for endometrial cell regeneration; (iv) shifting the treatment paradigm for all tumour types that rely on nerve cell innervation, (v) development and implementation of the world's first real-time patient treatment verification system (Watchdog); (vi) inventing the effective 'EAT' psychological intervention to improve nutrition and outcomes in people experiencing radiotherapy for head and neck cancer; (vi) developing effective interventions to reduce smoking rates among priority groups, currently being rolled out to disadvantaged populations in NSW; and (vii) establishing a Consumer Advisory Panel and Consumer Engagement Committee to increase consumer involvement in research. Conclusion: Using FAIT methodology, we have demonstrated the significant impact and downstream benefits that can be achieved by the provision of infrastructure-type funding to regional and rural research collaboratives to help address inequities in research activity and health outcomes and demonstrates a positive return on investment.
MeSH term(s)	Humans ; Program Evaluation/methods ; Translational Research, Biomedical ; Australia ; Translational Science, Biomedical ; Neoplasms/therapy
Language	English
Publishing date	2024-03-11
Publishing country	England
Document type	Journal Article
ZDB-ID	2050434-2
ISSN	1472-6963 ; 1472-6963
ISSN (online)	1472-6963
ISSN	1472-6963
DOI	10.1186/s12913-024-10680-2
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Article ; Online: Protein phosphatase 2A (PP2A): a key phosphatase in the progression of chronic obstructive pulmonary disease (COPD) to lung cancer.

Nader, Cassandra P / Cidem, Aylin / Verrills, Nicole M / Ammit, Alaina J

Respiratory research

2019 Volume 20, Issue 1, Page(s) 222

Abstract: Lung cancer (LC) has the highest relative risk of development as a comorbidity of chronic obstructive pulmonary disease (COPD). The molecular mechanisms that mediate chronic inflammation and lung function impairment in COPD have been identified in LC. ... ...

Abstract	Lung cancer (LC) has the highest relative risk of development as a comorbidity of chronic obstructive pulmonary disease (COPD). The molecular mechanisms that mediate chronic inflammation and lung function impairment in COPD have been identified in LC. This suggests the two diseases are more linked than once thought. Emerging data in relation to a key phosphatase, protein phosphatase 2A (PP2A), and its regulatory role in inflammatory and tumour suppression in both disease settings suggests that it may be critical in the progression of COPD to LC. In this review, we uncover the importance of the functional and active PP2A holoenzyme in the context of both diseases. We describe PP2A inactivation via direct and indirect means and explore the actions of two key PP2A endogenous inhibitors, cancerous inhibitor of PP2A (CIP2A) and inhibitor 2 of PP2A (SET), and the role they play in COPD and LC. We explain how dysregulation of PP2A in COPD creates a favourable inflammatory micro-environment and promotes the initiation and progression of tumour pathogenesis. Finally, we highlight PP2A as a druggable target in the treatment of COPD and LC and demonstrate the potential of PP2A re-activation as a strategy to halt COPD disease progression to LC. Although further studies are required to elucidate if PP2A activity in COPD is a causal link for LC progression, studies focused on the potential of PP2A reactivating agents to reduce the risk of LC formation in COPD patients will be pivotal in improving clinical outcomes for both COPD and LC patients in the future.
MeSH term(s)	Animals ; Autoantigens/administration & dosage ; Disease Progression ; Humans ; Intracellular Signaling Peptides and Proteins/administration & dosage ; Lung Neoplasms/diagnosis ; Lung Neoplasms/drug therapy ; Lung Neoplasms/enzymology ; Membrane Proteins/administration & dosage ; Protein Phosphatase 2/antagonists & inhibitors ; Protein Phosphatase 2/metabolism ; Pulmonary Disease, Chronic Obstructive/diagnosis ; Pulmonary Disease, Chronic Obstructive/drug therapy ; Pulmonary Disease, Chronic Obstructive/enzymology
Chemical Substances	Autoantigens ; CIP2A protein, human ; Intracellular Signaling Peptides and Proteins ; Membrane Proteins ; Protein Phosphatase 2 (EC 3.1.3.16)
Language	English
Publishing date	2019-10-17
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2041675-1
ISSN	1465-993X ; 1465-993X
ISSN (online)	1465-993X
ISSN	1465-993X
DOI	10.1186/s12931-019-1192-x
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Article ; Online: Harnessing the power of proteomics for identification of oncogenic, druggable signalling pathways in cancer.

Murray, Heather C / Dun, Matthew D / Verrills, Nicole M

Expert opinion on drug discovery

2017 Volume 12, Issue 5, Page(s) 431–447

Abstract: Introduction: Genomic and transcriptomic profiling of tumours has revolutionised our understanding of cancer. However, the majority of tumours possess multiple mutations, and determining which oncogene, or even which pathway, to target is difficult. ... ...

Abstract	Introduction: Genomic and transcriptomic profiling of tumours has revolutionised our understanding of cancer. However, the majority of tumours possess multiple mutations, and determining which oncogene, or even which pathway, to target is difficult. Proteomics is emerging as a powerful approach to identify the functionally important pathways driving these cancers, and how they can be targeted therapeutically. Areas covered: The authors provide a technical overview of mass spectrometry based approaches for proteomic profiling, and review the current and emerging strategies available for the identification of dysregulated networks, pathways, and drug targets in cancer cells, with a key focus on the ability to profile cancer kinomes. The potential applications of mass spectrometry in the clinic are also highlighted. Expert opinion: The addition of proteomic information to genomic platforms - 'proteogenomics' - is providing unparalleled insight in cancer cell biology. Application of improved mass spectrometry technology and methodology, in particular the ability to analyse post-translational modifications (the PTMome), is providing a more complete picture of the dysregulated networks in cancer, and uncovering novel therapeutic targets. While the application of proteomics to discovery research will continue to rise, improved workflow standardisation and reproducibility is required before mass spectrometry can enter routine clinical use.
MeSH term(s)	Animals ; Antineoplastic Agents/pharmacology ; Genomics/methods ; Humans ; Mass Spectrometry/methods ; Molecular Targeted Therapy ; Neoplasms/drug therapy ; Neoplasms/genetics ; Neoplasms/pathology ; Oncogenes/genetics ; Protein Processing, Post-Translational ; Proteomics/methods ; Reproducibility of Results ; Signal Transduction/drug effects
Chemical Substances	Antineoplastic Agents
Language	English
Publishing date	2017-05
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2259618-5
ISSN	1746-045X ; 1746-0441
ISSN (online)	1746-045X
ISSN	1746-0441
DOI	10.1080/17460441.2017.1304377
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Article: Ppp2r2a

Panicker, Nikita / Coutman, Melody / Lawlor-O'Neill, Charley / Kahl, Richard G S / Roselli, Séverine / Verrills, Nicole M

Frontiers in cell and developmental biology

2020 Volume 8, Page(s) 358

Abstract: The serine/threonine protein phosphatase 2A (PP2A) is a master regulator of the complex cellular signaling that occurs during all stages of mammalian development. PP2A is composed of a catalytic, a structural, and regulatory subunit, for which there are ... ...

Abstract	The serine/threonine protein phosphatase 2A (PP2A) is a master regulator of the complex cellular signaling that occurs during all stages of mammalian development. PP2A is composed of a catalytic, a structural, and regulatory subunit, for which there are multiple isoforms. The association of specific regulatory subunits determines substrate specificity and localization of phosphatase activity, however, the precise role of each regulatory subunit in development is not known. Here we report the generation of the first knockout mouse for the
Language	English
Publishing date	2020-06-05
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2737824-X
ISSN	2296-634X
ISSN	2296-634X
DOI	10.3389/fcell.2020.00358
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