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Article ; Online: Systematic Analysis of FASTK Gene Family Alterations in Cancer.

Magraner-Pardo, Lorena / Gobelli, Dino / de la Fuente, Miguel A / Pons, Tirso / Simarro, María

International journal of molecular sciences

2021 Volume 22, Issue 21

Abstract: The FASTK family of proteins have been recently reported to play a key role in the post-transcriptional regulation of mitochondrial gene expression, including mRNA stability and translation. Accumulated studies have provided evidence that the expression ... ...

Abstract	The FASTK family of proteins have been recently reported to play a key role in the post-transcriptional regulation of mitochondrial gene expression, including mRNA stability and translation. Accumulated studies have provided evidence that the expression of some FASTK genes is altered in certain types of cancer, in agreement with the central role of mitochondria in cancer development. Here, we obtained a pan-cancer overview of the genomic and transcriptomic alterations of FASTK genes. FASTK, FASTKD1, FASTKD3 and FASTKD5 showed the highest rates of genetic alterations. FASTK and FASTKD3 alterations consisted mainly of amplifications that were seen in more than 8% of ovarian and lung cancers, respectively. FASTKD1 and FASTKD5 were the most frequently mutated FASTK genes, and the mutations were identified in 5-7% of uterine cancers, as well as in 4% of melanomas. Our results also showed that the mRNA levels of all FASTK members were strongly upregulated in esophageal, stomach, liver and lung cancers. Finally, the protein-protein interaction network for FASTK proteins uncovers the interaction of FASTK, FASTKD2, FASTKD4 and FASTKD5 with cancer signaling pathways. These results serve as a starting point for future research into the potential of the FASTK family members as diagnostic and therapeutic targets for certain types of cancer.
MeSH term(s)	Databases, Genetic ; Gene Expression Regulation, Neoplastic ; Humans ; Mitochondria/genetics ; Mitochondria/metabolism ; Mutation ; Neoplasms/genetics ; Neoplasms/metabolism ; Protein Interaction Maps/genetics ; Protein Serine-Threonine Kinases/genetics ; Protein Serine-Threonine Kinases/metabolism ; RNA, Messenger/metabolism ; Signal Transduction/genetics ; Transcriptome/genetics
Chemical Substances	RNA, Messenger ; FASTK protein, human (EC 2.7.1.11) ; Protein Serine-Threonine Kinases (EC 2.7.11.1)
Language	English
Publishing date	2021-10-20
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms222111337
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Development of a novel in vitro model to study the modulatory role of the respiratory complex I in macrophage effector functions.

Serrano-Lorenzo, Pablo / Gobelli, Dino / Garrido-Moraga, Rocío / Esteban-Amo, María J / López-López, José R / Orduña, Antonio / de la Fuente, Miguel A / Martín, Miguel A / Simarro, María

PloS one

2023 Volume 18, Issue 9, Page(s) e0291442

Abstract: Increasing evidence demonstrate that the electron transfer chain plays a critical role in controlling the effector functions of macrophages. In this work, we have generated a Ndufs4-/- murine macrophage cell lines. The Ndufs4 gene, which encodes a ... ...

Abstract	Increasing evidence demonstrate that the electron transfer chain plays a critical role in controlling the effector functions of macrophages. In this work, we have generated a Ndufs4-/- murine macrophage cell lines. The Ndufs4 gene, which encodes a supernumerary subunit of complex I, is a mutational hotspot in Leigh syndrome patients. Ndufs4-/- macrophages showed decreased complex I activity, altered complex I assembly, and lower levels of maximal respiration and ATP production. These mitochondrial respiration alterations were associated with a shift towards a pro-inflammatory cytokine profile after lipopolysaccharide challenge and improved ability to phagocytose Gram-negative bacteria.
MeSH term(s)	Humans ; Animals ; Mice ; Electron Transport Complex I/genetics ; Macrophages ; Phagocytosis ; Cell Line ; Leigh Disease
Chemical Substances	Electron Transport Complex I (EC 7.1.1.2) ; Ndufs4 protein, mouse
Language	English
Publishing date	2023-09-19
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2267670-3
ISSN	1932-6203 ; 1932-6203
ISSN (online)	1932-6203
ISSN	1932-6203
DOI	10.1371/journal.pone.0291442
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Article ; Online: Characterization of endogenous Kv1.3 channel isoforms in T cells.

Serna, Julia / Peraza, Diego A / Moreno-Estar, Sara / Saez, Juan J / Gobelli, Dino / Simarro, Maria / Hivroz, Claire / López-López, José R / Cidad, Pilar / de la Fuente, Miguel A / Pérez-García, M Teresa

Journal of cellular physiology

2023 Volume 238, Issue 5, Page(s) 976–991

Abstract: Voltage-dependent potassium channel Kv1.3 plays a key role on T-cell activation; however, lack of reliable antibodies has prevented its accurate detection under endogenous circumstances. To overcome this limitation, we created a Jurkat T-cell line with ... ...

Abstract	Voltage-dependent potassium channel Kv1.3 plays a key role on T-cell activation; however, lack of reliable antibodies has prevented its accurate detection under endogenous circumstances. To overcome this limitation, we created a Jurkat T-cell line with endogenous Kv1.3 channel tagged, to determine the expression, location, and changes upon activation of the native Kv1.3 channels. CRISPR-Cas9 technique was used to insert a Flag-Myc peptide at the C terminus of the KCNA3 gene. Basal or activated channel expression was studied using western blot analysis and imaging techniques. We identified two isoforms of Kv1.3 other than the canonical channel (54 KDa) differing on their N terminus: a longer isoform (70 KDa) and a truncated isoform (43 KDa). All three isoforms were upregulated after T-cell activation. We focused on the functional characterization of the truncated isoform (short form, SF), because it has not been previously described and could be present in the available Kv1.3-/- mice models. Overexpression of SF in HEK cells elicited small amplitude Kv1.3-like currents, which, contrary to canonical Kv1.3, did not induce HEK proliferation. To explore the role of endogenous SF isoform in a native system, we generated both a knockout Jurkat clone and a clone expressing only the SF isoform. Although the canonical isoform (long form) localizes mainly at the plasma membrane, SF remains intracellular, accumulating perinuclearly. Accordingly, SF Jurkat cells did not show Kv1.3 currents and exhibited depolarized resting membrane potential (V
MeSH term(s)	Animals ; Humans ; Mice ; Cell Line ; Cell Membrane/metabolism ; Jurkat Cells ; Protein Isoforms/genetics ; Protein Isoforms/metabolism ; Kv1.3 Potassium Channel/genetics ; Kv1.3 Potassium Channel/metabolism
Chemical Substances	Protein Isoforms ; Kv1.3 Potassium Channel
Language	English
Publishing date	2023-02-28
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.30984
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Article ; Online: Impact of Metabolism on Immune Responses.

Elkhal, Abdallah / Rodriguez Cetina Biefer, Hector / de la Fuente, Miguel A

Journal of immunology research

2018 Volume 2018, Page(s) 5069316

MeSH term(s)	Animals ; Asthma/immunology ; Cellular Reprogramming ; Dendritic Cells/immunology ; Estrogens/metabolism ; Humans ; Immune System/metabolism ; Immunity ; Lipid Metabolism ; Obesity/immunology ; Th1 Cells/immunology ; Toll-Like Receptors/metabolism
Chemical Substances	Estrogens ; Toll-Like Receptors
Language	English
Publishing date	2018-07-26
Publishing country	Egypt
Document type	Editorial ; Introductory Journal Article
ZDB-ID	2817541-4
ISSN	2314-7156 ; 2314-8861
ISSN (online)	2314-7156
ISSN	2314-8861
DOI	10.1155/2018/5069316
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Article ; Online: Novel fluorescent-based reporter cell line engineered for monitoring homologous recombination events.

Bernardi, Alejandra / Gobelli, Dino / Serna, Julia / Nawrocka, Paulina / March-Rosselló, Gabriel / Orduña, Antonio / Kozlowski, Piotr / Simarro, María / de la Fuente, Miguel A

PloS one

2021 Volume 16, Issue 4, Page(s) e0237413

Abstract: Homologous recombination (HR) faithfully restores DNA double-strand breaks. Defects in this HR repair pathway are associated with cancer predisposition. In genetic engineering, HR has been used extensively to study gene function and it represents an ... ...

Abstract	Homologous recombination (HR) faithfully restores DNA double-strand breaks. Defects in this HR repair pathway are associated with cancer predisposition. In genetic engineering, HR has been used extensively to study gene function and it represents an ideal method of gene therapy for single gene disorders. Here, we present a novel assay to measure HR in living cells. The HR substrate consisted of a non-fluorescent 3' truncated form of the eGFP gene and was integrated into the AAVS1 locus, known as a safe harbor. The donor DNA template comprised a 5' truncated eGFP copy and was delivered via AAV particles. HR mediated repair restored full-length eGFP coding sequence, resulting in eGFP+ cells. The utility of our assay in quantifying HR events was validated by exploring the impact of the overexpression of HR promoters and the siRNA-mediated silencing of genes known to play a role in DNA repair on the frequency of HR. We conclude that this novel assay represents a useful tool to further investigate the mechanisms that control HR and test continually emerging tools for HR-mediated genome editing.
MeSH term(s)	Cell Line ; Cell Line, Tumor ; DNA Breaks, Double-Stranded ; DNA End-Joining Repair/genetics ; Fluorescence ; Genetic Engineering/methods ; Green Fluorescent Proteins/genetics ; HCT116 Cells ; HEK293 Cells ; Homologous Recombination/genetics ; Humans ; Neoplasms/genetics ; Promoter Regions, Genetic/genetics ; Recombinational DNA Repair/genetics
Chemical Substances	Green Fluorescent Proteins (147336-22-9)
Language	English
Publishing date	2021-04-30
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0237413
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Article: Unilateral birdshot-like choroidopathy: a case report.

de la Fuente, Miguel A / Recio, Pilar

Retinal cases & brief reports

2012 Volume 6, Issue 4, Page(s) 365–367

Abstract: Purpose: To report on an unusual case of unilateral birdshot-like choroidopathy and to describe its clinical characteristics.: Methods: Prospective follow-up study of clinical, laboratory, electrophysiologic, and angiographic evolution of a patient ... ...

Abstract	Purpose: To report on an unusual case of unilateral birdshot-like choroidopathy and to describe its clinical characteristics. Methods: Prospective follow-up study of clinical, laboratory, electrophysiologic, and angiographic evolution of a patient with choroidal lesions mimicking birdshot chorioretinitis. Main outcomes measures: Visual acuity, serial visual fields, spectral domain optical coherent tomography, electrophysiologic studies: full-field electroretinogram, pattern electroretinogram, multifocal electroretinogram, and electrooculogram. Fluorescein angiography, indocyanine green angiography, color vision and contrast sensitivity studies. Patients/design: Observational case report. Results: At 30 months of follow-up, visual acuity was 20/20 in both eyes. There were no signs of intraocular inflammation at any time over follow-up. Serial visual field showed no abnormality. Electrophysiologic studies reflected normal retinal function. Color vision and contrast sensitivity were both normal. Fluorescein angiography depicted unilateral hypofluorescent choroidal spots in early phases becoming hyperfluorescent in late frames without changes over follow-up. Indocyanine green angiography pointed out diffuse hypofluorescent choroidal lesions in early and late frames that did not modify over follow-up. Conclusions: We present an interesting but unusual case of idiopathic unilateral choroidal lesions mimicking those seen in birdshot chorioretinitis but without evidence of active inflammation. Our case has been called unilateral birdshot-like choroidopathy on the basis of the characteristics of the lesions and the lack of active inflammation. The patient has been followed up for 30 months without treatment, and no changes in visual function or clinical features have been observed. Clinicians should be aware of the diagnostic criteria of birdshot chorioretinitis to avoid unnecessary treatment of patients with other diseases mimicking birdshot.
Language	English
Publishing date	2012
Publishing country	United States
Document type	Journal Article
ISSN	1935-1089
ISSN	1935-1089
DOI	10.1097/ICB.0b013e31824f7107
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Article: Mitochondrial Complex I Dysfunction and Peripheral Chemoreflex Sensitivity in a FASTK-Deficient Mice Model.

Gomez-Niño, Angela / Docio, Inmaculada / Prieto-Lloret, Jesus / Simarro, Maria / de la Fuente, Miguel A / Rocher, Asuncion

Advances in experimental medicine and biology

2018 Volume 1071, Page(s) 51–59

Abstract: The molecular mechanisms underlying ... ...

Abstract	The molecular mechanisms underlying O
MeSH term(s)	Animals ; Carotid Body/physiology ; Electron Transport Complex I/metabolism ; Hypercapnia/physiopathology ; Hypoxia/physiopathology ; Mice ; Mice, Knockout ; Mitochondria ; Protein-Serine-Threonine Kinases/genetics ; Protein-Serine-Threonine Kinases/metabolism
Chemical Substances	Electron Transport Complex I (EC 1.6.5.3) ; Protein-Serine-Threonine Kinases (EC 2.7.11.1)
Language	English
Publishing date	2018-11-13
Publishing country	United States
Document type	Journal Article
ISSN	2214-8019 ; 0065-2598
ISSN (online)	2214-8019
ISSN	0065-2598
DOI	10.1007/978-3-319-91137-3_6
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Article ; Online: Voltage-dependent conformational changes of Kv1.3 channels activate cell proliferation.

Cidad, Pilar / Alonso, Esperanza / Arévalo-Martínez, Marycarmen / Calvo, Enrique / de la Fuente, Miguel A / Pérez-García, M Teresa / López-López, José R

Journal of cellular physiology

2020 Volume 236, Issue 6, Page(s) 4330–4347

Abstract: The voltage-dependent potassium channel Kv1.3 has been implicated in proliferation in many cell types, based on the observation that Kv1.3 blockers inhibited proliferation. By modulating membrane potential, cell volume, and/or ... ...

Abstract	The voltage-dependent potassium channel Kv1.3 has been implicated in proliferation in many cell types, based on the observation that Kv1.3 blockers inhibited proliferation. By modulating membrane potential, cell volume, and/or Ca
MeSH term(s)	Cell Proliferation ; GTPase-Activating Proteins/genetics ; GTPase-Activating Proteins/metabolism ; HEK293 Cells ; Humans ; Ion Channel Gating ; KATP Channels/genetics ; KATP Channels/metabolism ; Kv1.3 Potassium Channel/chemistry ; Kv1.3 Potassium Channel/genetics ; Kv1.3 Potassium Channel/metabolism ; Membrane Potentials ; Muscle, Smooth, Vascular/metabolism ; Mutation ; Myocytes, Smooth Muscle/metabolism ; Protein Conformation ; Signal Transduction ; Structure-Activity Relationship
Chemical Substances	GTPase-Activating Proteins ; IQGAP3 protein, human ; KATP Channels ; KCNA3 protein, human ; Kv1.3 Potassium Channel
Language	English
Publishing date	2020-11-23
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.30170
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Article ; Online: Unilateral acute idiopathic maculopathy: angiography, optical coherence tomography and microperimetry findings.

de la Fuente, Miguel A / Cuadrado, Rubén

Journal of ophthalmic inflammation and infection

2010 Volume 1, Issue 3, Page(s) 125–127

Abstract: Unilateral acute idiopathic maculopathy (UAIM) is an uncommon inflammatory disease of the retinal pigment epithelium (RPE) that affects young adults. The variability of clinical features of UAIM makes the diagnosis cumbersome. We report on a 25-year-old ... ...

Abstract	Unilateral acute idiopathic maculopathy (UAIM) is an uncommon inflammatory disease of the retinal pigment epithelium (RPE) that affects young adults. The variability of clinical features of UAIM makes the diagnosis cumbersome. We report on a 25-year-old man with sudden loss of visual acuity (VA) and a central scotoma in his right eye. Fluorescein angiography localised the lesion in the RPE. Microperimetry revealed a central scotoma extending beyond the lesion margins with complete recovery of retinal sensitivity over weeks. Optical coherence tomography at presentation showed a thickened RPE. We are unaware of previous reports of UAIM studied by microperimetry and could find no reference to it in a computerised search using MEDLINE.
Language	English
Publishing date	2010-11-24
Publishing country	Germany
Document type	Journal Article
ZDB-ID	2592309-2
ISSN	1869-5760 ; 1869-5760
ISSN (online)	1869-5760
ISSN	1869-5760
DOI	10.1007/s12348-010-0014-6
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Article ; Online: The FASTK family of proteins: emerging regulators of mitochondrial RNA biology.

Jourdain, Alexis A / Popow, Johannes / de la Fuente, Miguel A / Martinou, Jean-Claude / Anderson, Paul / Simarro, Maria

Nucleic acids research

2017 Volume 45, Issue 19, Page(s) 10941–10947

Abstract: The FASTK family proteins have recently emerged as key post-transcriptional regulators of mitochondrial gene expression. FASTK, the founding member and its homologs FASTKD1-5 are architecturally related RNA-binding proteins, each having a different ... ...

Abstract	The FASTK family proteins have recently emerged as key post-transcriptional regulators of mitochondrial gene expression. FASTK, the founding member and its homologs FASTKD1-5 are architecturally related RNA-binding proteins, each having a different function in the regulation of mitochondrial RNA biology, from mRNA processing and maturation to ribosome assembly and translation. In this review, we outline the structure, evolution and function of these FASTK proteins and discuss the individual role that each has in mitochondrial RNA biology. In addition, we highlight the aspects of FASTK research that still require more attention.
MeSH term(s)	Gene Expression Regulation ; Humans ; Mitochondrial Proteins/genetics ; Mitochondrial Proteins/metabolism ; Protein-Serine-Threonine Kinases/genetics ; Protein-Serine-Threonine Kinases/metabolism ; RNA/genetics ; RNA/metabolism ; RNA, Messenger/genetics ; RNA, Messenger/metabolism ; RNA, Mitochondrial ; RNA-Binding Proteins/genetics ; RNA-Binding Proteins/metabolism
Chemical Substances	FASTKD1 protein, human ; Mitochondrial Proteins ; RNA, Messenger ; RNA, Mitochondrial ; RNA-Binding Proteins ; TBRG4 protein, human ; RNA (63231-63-0) ; FASTKD2 protein, human (EC 2.7.11.1) ; FASTKD3 protein, human (EC 2.7.11.1) ; Protein-Serine-Threonine Kinases (EC 2.7.11.1)
Language	English
Publishing date	2017-10-06
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	186809-3
ISSN	1362-4962 ; 1362-4954 ; 0301-5610 ; 0305-1048
ISSN (online)	1362-4962 ; 1362-4954
ISSN	0301-5610 ; 0305-1048
DOI	10.1093/nar/gkx772
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