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Article: Correction to: Survival of midbrain dopamine neurons depends on the Bcl2 factor Mcl1.

Robinson, Edward J / Aguiar, Sebastian P / Kouwenhoven, Willemieke M / Starmans, Dorinde S / von Oerthel, Lars / Smidt, Marten P / van der Heide, Lars P

Cell death discovery

2022 Volume 8, Issue 1, Page(s) 102

Language	English
Publishing date	2022-03-07
Publishing country	United States
Document type	Published Erratum
ISSN	2058-7716
ISSN	2058-7716
DOI	10.1038/s41420-022-00871-3
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Article ; Online: Tyrosine hydroxylase phosphorylation is under the control of serine 40.

Stoop, Jesse / Douma, Erik H / van der Vlag, Marc / Smidt, Marten P / van der Heide, Lars P

Journal of neurochemistry

2023 Volume 167, Issue 3, Page(s) 376–393

Abstract: Tyrosine hydroxylase catalyzes the initial and rate-limiting step in the biosynthesis of the neurotransmitter dopamine. The phosphorylation state of Ser40 and Ser31 is believed to exert a direct effect on the enzymatic activity of tyrosine hydroxylase. ... ...

Abstract	Tyrosine hydroxylase catalyzes the initial and rate-limiting step in the biosynthesis of the neurotransmitter dopamine. The phosphorylation state of Ser40 and Ser31 is believed to exert a direct effect on the enzymatic activity of tyrosine hydroxylase. Interestingly, some studies report that Ser31 phosphorylation affects Ser40 phosphorylation, while Ser40 phosphorylation has no effect on Ser31 phosphorylation, a process named hierarchical phosphorylation. Here, we provide a detailed investigation into the signal transduction mechanisms regulating Ser40 and Ser31 phosphorylation in dopaminergic mouse MN9D and Neuro2A cells. We find that cyclic nucleotide signaling drives Ser40 phosphorylation, and that Ser31 phosphorylation is strongly regulated by ERK signaling. Inhibition of ERK1/2 with UO126 or PD98059 reduced Ser31 phosphorylation, but surprisingly had no effect on Ser40 phosphorylation, contradicting a role for Ser31 in the regulation of Ser40. Moreover, to elucidate a possible hierarchical mechanism controlling tyrosine hydroxylase phosphorylation, we introduced tyrosine hydroxylase variants in Neuro2A mouse neuroblastoma cells that mimic either phosphorylated or unphosphorylated serine residues. When we introduced a Ser40Ala tyrosine hydroxylase variant, Ser31 phosphorylation was completely absent. Additionally, neither the tyrosine hydroxylase variant Ser31Asp, nor the variant Ser31Ala had any significant effect on basal Ser40 phosphorylation levels. These results suggest that tyrosine hydroxylase is not controlled by hierarchical phosphorylation in the sense that first Ser31 has to be phosphorylated and subsequently Ser40, but, conversely, that Ser40 phosphorylation is essential for Ser31 phosphorylation. Overall our study suggests that Ser40 is the crucial residue to target so as to modulate tyrosine hydroxylase activity.
Language	English
Publishing date	2023-09-30
Publishing country	England
Document type	Journal Article
ZDB-ID	80158-6
ISSN	1471-4159 ; 0022-3042 ; 1474-1644
ISSN (online)	1471-4159
ISSN	0022-3042 ; 1474-1644
DOI	10.1111/jnc.15963
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Article: NUAK1 and NUAK2 Fine-Tune TGF-β Signaling.

van de Vis, Reinofke A J / Moustakas, Aristidis / van der Heide, Lars P

Cancers

2021 Volume 13, Issue 13

Abstract: Transforming growth factor-β (TGF-β) signaling plays a key role in governing various cellular processes, extending from cell proliferation and apoptosis to differentiation and migration. Due to this extensive involvement in the regulation of cellular ... ...

Abstract	Transforming growth factor-β (TGF-β) signaling plays a key role in governing various cellular processes, extending from cell proliferation and apoptosis to differentiation and migration. Due to this extensive involvement in the regulation of cellular function, aberrant TGF-β signaling is frequently implicated in the formation and progression of tumors. Therefore, a full understanding of the mechanisms of TGF-β signaling and its key components will provide valuable insights into how this intricate signaling cascade can shift towards a detrimental course. In this review, we discuss the interplay between TGF-β signaling and the AMP-activated protein kinase (AMPK)-related NUAK kinase family. We highlight the function and regulation of these kinases with focus on the pivotal role NUAK1 and NUAK2 play in regulating TGF-β signaling. Specifically, TGF-β induces the expression of NUAK1 and NUAK2 that regulates TGF-β signaling output in an opposite manner. Besides the focus on the TGF-β pathway, we also present a broader perspective on the expression and signaling interactions of the NUAK kinases to outline the broader functions of these protein kinases.
Language	English
Publishing date	2021-07-05
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2527080-1
ISSN	2072-6694
ISSN	2072-6694
DOI	10.3390/cancers13133377
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Article ; Online: MCL1 as a Therapeutic Target in Parkinson's Disease?

Robinson, Edward J / Aguiar, Sebastian / Smidt, Marten P / van der Heide, Lars P

Trends in molecular medicine

2019 Volume 25, Issue 12, Page(s) 1056–1065

Abstract: Dopamine neurons in the substantia nigra (SN) pars compacta are selectively lost during the progression of Parkinson's disease (PD). Recent work performed on the role of the Bcl2 family (highly specialized proteins which control cellular survival and ... ...

Abstract	Dopamine neurons in the substantia nigra (SN) pars compacta are selectively lost during the progression of Parkinson's disease (PD). Recent work performed on the role of the Bcl2 family (highly specialized proteins which control cellular survival and death) in midbrain dopamine neurons has led to the identification of the Bcl2 factor Mcl1 as a weak link in the survival of these neurons. We hypothesize that the regulation of BCL2 proteins may explain this selective vulnerability, and may even provide a novel therapeutic opportunity - strengthening weak links such as MCL1 could result in a delay or complete abrogation of cell death during PD.
MeSH term(s)	Animals ; Cell Death/drug effects ; Dopaminergic Neurons/metabolism ; Dopaminergic Neurons/pathology ; Humans ; Molecular Targeted Therapy ; Myeloid Cell Leukemia Sequence 1 Protein/metabolism ; Parkinson Disease/drug therapy ; Parkinson Disease/metabolism ; Parkinson Disease/pathology ; Peptides/pharmacology ; Proteasome Endopeptidase Complex/metabolism ; Proto-Oncogene Proteins c-bcl-2/metabolism ; Small Molecule Libraries/pharmacology ; Substantia Nigra/metabolism ; Substantia Nigra/pathology ; Ubiquitin/metabolism
Chemical Substances	MCL1 protein, human ; Myeloid Cell Leukemia Sequence 1 Protein ; Peptides ; Proto-Oncogene Proteins c-bcl-2 ; Small Molecule Libraries ; Ubiquitin ; Proteasome Endopeptidase Complex (EC 3.4.25.1)
Language	English
Publishing date	2019-11-06
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2036490-8
ISSN	1471-499X ; 1471-4914
ISSN (online)	1471-499X
ISSN	1471-4914
DOI	10.1016/j.molmed.2019.08.009
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Article ; Online: Transforming growth factor β (TGFβ) induces NUAK kinase expression to fine-tune its signaling output.

Kolliopoulos, Constantinos / Raja, Erna / Razmara, Masoud / Heldin, Paraskevi / Heldin, Carl-Henrik / Moustakas, Aristidis / van der Heide, Lars P

The Journal of biological chemistry

2019 Volume 294, Issue 11, Page(s) 4119–4136

Abstract: TGFβ signaling via SMAD proteins and protein kinase pathways up- or down-regulates the expression of many genes and thus affects physiological processes, such as differentiation, migration, cell cycle arrest, and apoptosis, during developmental or adult ... ...

Abstract	TGFβ signaling via SMAD proteins and protein kinase pathways up- or down-regulates the expression of many genes and thus affects physiological processes, such as differentiation, migration, cell cycle arrest, and apoptosis, during developmental or adult tissue homeostasis. We here report that NUAK family kinase 1 (
MeSH term(s)	Cells, Cultured ; Gene Expression Profiling ; Humans ; Protein Kinases/genetics ; Protein Kinases/metabolism ; Protein-Serine-Threonine Kinases/genetics ; Protein-Serine-Threonine Kinases/metabolism ; Real-Time Polymerase Chain Reaction ; Repressor Proteins/genetics ; Repressor Proteins/metabolism ; Signal Transduction/genetics ; Transforming Growth Factor beta/metabolism
Chemical Substances	Repressor Proteins ; Transforming Growth Factor beta ; Protein Kinases (EC 2.7.-) ; NUAK1 protein, human (EC 2.7.1.-) ; NUAK2 protein, human (EC 2.7.11.1) ; Protein-Serine-Threonine Kinases (EC 2.7.11.1)
Language	English
Publishing date	2019-01-08
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2997-x
ISSN	1083-351X ; 0021-9258
ISSN (online)	1083-351X
ISSN	0021-9258
DOI	10.1074/jbc.RA118.004984
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Article: Survival of midbrain dopamine neurons depends on the Bcl2 factor Mcl1.

Robinson, Edward J / Aguiar, Sebastian P / Kouwenhoven, Willemieke M / Starmans, Dorinde S / von Oerthel, Lars / Smidt, Marten P / van der Heide, Lars P

Cell death discovery

2018 Volume 4, Page(s) 107

Abstract: Mitochondria-dependent apoptosis plays an important role in the embryonic development of the midbrain dopaminergic system as well as in Parkinson's disease. Central to mitochondria-dependent apoptosis is the Bcl2 family of apoptosis-regulating proteins. ... ...

Abstract	Mitochondria-dependent apoptosis plays an important role in the embryonic development of the midbrain dopaminergic system as well as in Parkinson's disease. Central to mitochondria-dependent apoptosis is the Bcl2 family of apoptosis-regulating proteins. However, it was unclear which Bcl2 proteins are important for the survival of dopaminergic neurons. Here, we identify Mcl1 as a critical Bcl2 pro-survival factor in midbrain dopaminergic neurons. Using a chemical biology approach to inhibit various components of the apoptotic machinery in the dopaminergic MN9D cell line or the control neuroblastoma N2A cell line, we find that functional inhibition of Mcl1 with the high affinity small molecule inhibitor UMI-77 results in a rapid and dose-dependent loss of viability, selectively in dopaminergic cells. In-depth analysis of the apoptotic signaling pathway reveals that chemical inhibition of Mcl1 results in the activation of Bax, activation of cleaved caspase-3 and finally cell death. The dependence of mouse dopaminergic midbrain neurons on Mcl1 was confirmed using ex vivo slice cultures from Pitx3GFP/+ and wildtype mice. In mouse dopaminergic midbrain neurons positive for the midbrain dopaminergic marker Pitx3, or tyrosine hydroxylase, UMI-77 treatment caused a dramatic increase in cleaved caspase 3, indicating that Mcl1 activity is required for basal neuronal survival. Overall, our results suggest that Mcl1 is of critical importance to dopaminergic neurons and is a weak link in the chain controlling cellular survival. Boosting the pro-survival function of Mcl1 should be pursued as a therapeutic approach to augment the resilience of midbrain dopaminergic neurons to apoptotic stress in Parkinson's disease.
Language	English
Publishing date	2018-11-21
Publishing country	United States
Document type	Journal Article
ISSN	2058-7716
ISSN	2058-7716
DOI	10.1038/s41420-018-0125-7
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Article ; Online: The BCL2 code to dopaminergic development and Parkinson's disease.

van der Heide, Lars P / Smidt, Marten P

Trends in molecular medicine

2013 Volume 19, Issue 4, Page(s) 211–216

Abstract: Continuous, nonrandom cell death during development of the dopaminergic system is carefully orchestrated by locally secreted growth factors and the expression of transcription factors to ensure every neuron is carefully placed in its appropriate position ...

Abstract	Continuous, nonrandom cell death during development of the dopaminergic system is carefully orchestrated by locally secreted growth factors and the expression of transcription factors to ensure every neuron is carefully placed in its appropriate position and no 'miswiring' occurs. We hypothesize that the machinery directly responsible for executing cell death is composed of a precisely calibrated array of BCL2 proteins. Paradoxically, these BCL2 proteins, required for proper development of the dopaminergic system, may also cause vulnerability of this system in the adult, as these BCL2 proteins have recently been linked to Parkinson's disease. In addition to the intriguing possibility of finding useful biomarkers for predicting later neurodegeneration, further investigation of these factors could open new paths for treating Parkinson's disease.
MeSH term(s)	Adult ; Animals ; Cell Death ; Dopamine/metabolism ; Homeodomain Proteins/genetics ; Homeodomain Proteins/metabolism ; Humans ; Mitochondrial Diseases/genetics ; Neurons/metabolism ; Nuclear Receptor Subfamily 4, Group A, Member 2/genetics ; Nuclear Receptor Subfamily 4, Group A, Member 2/metabolism ; Parkinson Disease/genetics ; Proto-Oncogene Proteins c-bcl-2/genetics ; Proto-Oncogene Proteins c-bcl-2/metabolism ; Substantia Nigra/metabolism ; Transcription Factors/genetics ; Transcription Factors/metabolism ; Transcription, Genetic
Chemical Substances	Homeodomain Proteins ; NR4A2 protein, human ; Nuclear Receptor Subfamily 4, Group A, Member 2 ; Proto-Oncogene Proteins c-bcl-2 ; Transcription Factors ; homeobox protein PITX3 ; Dopamine (VTD58H1Z2X)
Language	English
Publishing date	2013-04
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2036490-8
ISSN	1471-499X ; 1471-4914
ISSN (online)	1471-499X
ISSN	1471-4914
DOI	10.1016/j.molmed.2013.02.003
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Article ; Online: FoxK2 is required for cellular proliferation and survival.

van der Heide, Lars P / Wijchers, Patrick J E C / von Oerthel, Lars / Burbach, J Peter H / Hoekman, Marco F M / Smidt, Marten P

Journal of cellular physiology

2014 Volume 230, Issue 5, Page(s) 1013–1023

Abstract: FoxK2 is a forkhead transcription factor expressed ubiquitously in the developing murine central nervous system. Here we investigated the role of FoxK2 in vitro and focused on proliferation and cellular survival. Knockdown of FoxK2 results in a decrease ... ...

Abstract	FoxK2 is a forkhead transcription factor expressed ubiquitously in the developing murine central nervous system. Here we investigated the role of FoxK2 in vitro and focused on proliferation and cellular survival. Knockdown of FoxK2 results in a decrease in BrdU incorporation and H3 phosphorylation, suggesting attenuation of proliferation. In the absence of growth factors, FoxK2 knockdown results in a dramatic increase in caspase 3 activity and propidium iodide positive cells, indicative of cell death. Additionally, knockdown of FoxK2 results in an increase in the mRNA of Gadd45α, Gadd45γ, as well as an increase in the phosphorylation of the mTOR dependent kinase p70S6K. Rapamycin treatment completely blocked the increase in p70S6K and synergistically potentiated the decrease in H3 phosphorylation upon FoxK2 knockdown. To gain more insight into the proapoptotic effects upon FoxK2 knockdown we screened for changes in Bcl2 genes. Upon FoxK2 knockdown both Puma and Noxa were significantly upregulated. Both genes were not inhibited by rapamycin treatment, instead rapamycin increased Noxa mRNA. FoxK2 requirement in cellular survival is further emphasized by the fact that resistance to TGFβ-induced cell death was greatly diminished after FoxK2 knockdown. Overall our data suggest FoxK2 is required for proliferation and survival, that mTOR is part of a feedback loop partly compensating for FoxK2 loss, possibly by upregulating Gadd45s, whereas cell death upon FoxK2 loss is induced in a Bcl2 dependent manner via Puma and Noxa.
MeSH term(s)	Animals ; Cell Death/drug effects ; Cell Proliferation/drug effects ; Cell Survival/drug effects ; Forkhead Transcription Factors/metabolism ; Gene Knockdown Techniques ; HEK293 Cells ; Histones/metabolism ; Humans ; Intracellular Signaling Peptides and Proteins/metabolism ; Intracellular Space/metabolism ; Mice ; Mice, Inbred C57BL ; Models, Biological ; NIH 3T3 Cells ; Phosphorylation/drug effects ; Protein Transport/drug effects ; Proto-Oncogene Proteins c-bcl-2/metabolism ; RNA, Small Interfering/metabolism ; Reproducibility of Results ; Ribosomal Protein S6 Kinases, 70-kDa/metabolism ; TOR Serine-Threonine Kinases/metabolism ; Transforming Growth Factor beta/pharmacology ; GADD45 Proteins
Chemical Substances	Forkhead Transcription Factors ; FoxK2 protein, mouse ; Histones ; Intracellular Signaling Peptides and Proteins ; Proto-Oncogene Proteins c-bcl-2 ; RNA, Small Interfering ; Transforming Growth Factor beta ; Ribosomal Protein S6 Kinases, 70-kDa (EC 2.7.11.1) ; TOR Serine-Threonine Kinases (EC 2.7.11.1)
Language	English
Publishing date	2014-09-14
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	3116-1
ISSN	1097-4652 ; 0021-9541
ISSN (online)	1097-4652
ISSN	0021-9541
DOI	10.1002/jcp.24828
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Article: Regulation of FoxO activity by CBP/p300-mediated acetylation.

van der Heide, Lars P / Smidt, Marten P

Trends in biochemical sciences

2005 Volume 30, Issue 2, Page(s) 81–86

Abstract: Forkhead box, class O (FoxO) transcription factors are inhibited by insulin-induced FoxO phosphorylation. Recently, acetylation of FoxO factors by calcium response element-binding (CREB)-binding protein (CBP) and/or p300 has been identified as a novel ... ...

Abstract	Forkhead box, class O (FoxO) transcription factors are inhibited by insulin-induced FoxO phosphorylation. Recently, acetylation of FoxO factors by calcium response element-binding (CREB)-binding protein (CBP) and/or p300 has been identified as a novel regulatory pathway, although the exact consequences of acetylation remain unclear. We propose that binding of CBP/p300 to FoxO factors is essential for FoxO-mediated transcription. CBP and p300 act as FoxO cofactors by weakening histone-DNA interactions. Acetylation of FoxO factors, however, attenuates FoxO-mediated transcriptional activity by disrupting the interaction between FoxO factors and target DNA. Therefore, acetylation shifts the function of FoxO from cell-cycle arrest and protection against oxidative stress towards cell death.
MeSH term(s)	Acetylation ; Animals ; CREB-Binding Protein ; DNA/metabolism ; Forkhead Transcription Factors ; Growth Substances/metabolism ; Histone Deacetylases/metabolism ; Histones/metabolism ; Humans ; Insulin/metabolism ; Models, Biological ; Nuclear Proteins/metabolism ; Nuclear Proteins/physiology ; Phosphorylation ; Protein Binding ; Sirtuins/metabolism ; Trans-Activators/metabolism ; Trans-Activators/physiology ; Transcription Factors/metabolism ; Transcription Factors/physiology
Chemical Substances	Forkhead Transcription Factors ; Growth Substances ; Histones ; Insulin ; Nuclear Proteins ; Trans-Activators ; Transcription Factors ; DNA (9007-49-2) ; CREB-Binding Protein (EC 2.3.1.48) ; CREBBP protein, human (EC 2.3.1.48) ; Sirtuins (EC 3.5.1.-) ; Histone Deacetylases (EC 3.5.1.98)
Language	English
Publishing date	2005-02
Publishing country	England
Document type	Journal Article
ZDB-ID	194216-5
ISSN	1362-4326 ; 0968-0004 ; 0376-5067
ISSN (online)	1362-4326
ISSN	0968-0004 ; 0376-5067
DOI	10.1016/j.tibs.2004.12.002
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Article ; Online: Lmx1a is an activator of Rgs4 and Grb10 and is responsible for the correct specification of rostral and medial mdDA neurons.

Hoekstra, Elisa J / von Oerthel, Lars / van der Linden, Annemarie J A / Schellevis, Raymond D / Scheppink, Gerard / Holstege, Frank C P / Groot-Koerkamp, Marian J / van der Heide, Lars P / Smidt, Marten P

The European journal of neuroscience

2013 Volume 37, Issue 1, Page(s) 23–32

Abstract: The LIM homeodomain transcription factor Lmx1a is a very potent inducer of stem cells towards dopaminergic neurons. Despite several studies on the function of this gene, the exact in vivo role of Lmx1a in mesodiencephalic dopamine (mdDA) neuronal ... ...

Abstract	The LIM homeodomain transcription factor Lmx1a is a very potent inducer of stem cells towards dopaminergic neurons. Despite several studies on the function of this gene, the exact in vivo role of Lmx1a in mesodiencephalic dopamine (mdDA) neuronal specification is still not understood. To analyse the genes functioning downstream of Lmx1a, we performed expression microarray analysis of LMX1A-overexpressing MN9D dopaminergic cells. Several interesting regulated genes were identified, based on their regulation in other previously generated expression arrays and on their expression pattern in the developing mdDA neuronal field. Post analysis through in vivo expression analysis in Lmx1a mouse mutant (dr/dr) embryos demonstrated a clear decrease in expression of the genes Grb10 and Rgs4, in and adjacent to the rostral and dorsal mdDA neuronal field and within the Lmx1a expression domain. Interestingly, the DA marker Vmat2 was significantly up-regulated as a consequence of increased LMX1A dose, and subsequent analysis on Lmx1a-mutant E14.5 and adult tissue revealed a significant decrease in Vmat2 expression in mdDA neurons. Taken together, microarray analysis of an LMX1A-overexpression cell system resulted in the identification of novel direct or indirect downstream targets of Lmx1a in mdDA neurons: Grb10, Rgs4 and Vmat2.
MeSH term(s)	Animals ; Brain/cytology ; Brain/embryology ; Brain/metabolism ; Cell Line ; Dopaminergic Neurons/metabolism ; GRB10 Adaptor Protein/genetics ; GRB10 Adaptor Protein/metabolism ; Gene Expression Profiling ; Gene Expression Regulation, Developmental ; LIM-Homeodomain Proteins/genetics ; LIM-Homeodomain Proteins/metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Mutant Strains ; Mutation ; Oligonucleotide Array Sequence Analysis ; RGS Proteins/genetics ; RGS Proteins/metabolism ; Transcription Factors/genetics ; Transcription Factors/metabolism ; Transcription, Genetic ; Vesicular Monoamine Transport Proteins/genetics ; Vesicular Monoamine Transport Proteins/metabolism
Chemical Substances	Grb10 protein, mouse ; LIM-Homeodomain Proteins ; Lmx1a protein, mouse ; RGS Proteins ; Slc18a2 protein, mouse ; Transcription Factors ; Vesicular Monoamine Transport Proteins ; GRB10 Adaptor Protein (151441-47-3) ; RGS4 protein (175335-35-0)
Language	English
Publishing date	2013-01
Publishing country	France
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	645180-9
ISSN	1460-9568 ; 0953-816X
ISSN (online)	1460-9568
ISSN	0953-816X
DOI	10.1111/ejn.12022
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