PUBLICACIÓN

Fluctuation in O-GlcNAcylation inactivates STIM1 to reduce store-operated calcium ion entry via down-regulation of Ser621phosphorylation

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ACCEDER A LA PUBLICACIÓN: Scopus Orcid

Atsuo Nomura, Shunichi Yokoe, Kiichiro Tomoda, Takatoshi Nakagawa, Francisco Javier Martin-Romero, Michio Asahi

2020 JOURNAL OF BIOLOGICAL CHEMISTRY

Biochemistry (Q1), Cell Biology (Q1), Molecular Biology (Q1)

JCR: 5.157

SJR: 2.361

CITAS

11

DOI

10.1074/jbc.ra120.014271

EID

2-s2.0-85097576217

ISSN

0021-9258

EISSN

1083-351X

BIBTEX

@article{Nomura_2020, doi = {10.1074/jbc.ra120.014271}, url = {https://doi.org/10.1074%2Fjbc.ra120.014271}, year = 2020, month = {dec}, publisher = {Elsevier {BV}}, volume = {295}, number = {50}, pages = {17071--17082}, author = {Atsuo Nomura and Shunichi Yokoe and Kiichiro Tomoda and Takatoshi Nakagawa and Francisco Javier Martin-Romero and Michio Asahi}, title = {Fluctuation in O-{GlcNAcylation} inactivates {STIM}1 to reduce store-operated calcium ion entry via down-regulation of Ser621 phosphorylation}, journal = {Journal of Biological Chemistry} }

AUTORES DE LA UEX

Francisco Javier Martín Romero

OTRAS PUBLICACIONES DE INTERÉS

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Stim1 Translocation To The Nucleus Protects Cells From Dna Damage
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Stim1 Translocation To The Nucleus Protects Cells From Dna Damage
Editorial: Molecular Components Of Store-Operated Calcium Entry In Health And Disease, Volume Ii
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Editorial: Molecular Components Of Store-Operated Calcium Entry In Health And Disease, Volume Ii
Internalized Amyloid-Β (1-42) Peptide Inhibits The Store-Operated Calcium Entry In Ht-22 Cells
Editorial: Molecular Components Of Store-Operated Calcium Entry In Health And Disease, Volume Ii
Internalized Amyloid-Β (1-42) Peptide Inhibits The Store-Operated Calcium Entry In Ht-22 Cells
Editorial: Molecular Components Of Store-Operated Calcium Entry In Health And Disease
Internalized Amyloid-Β (1-42) Peptide Inhibits The Store-Operated Calcium Entry In Ht-22 Cells
Editorial: Molecular Components Of Store-Operated Calcium Entry In Health And Disease
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Stim1 Deficiency Leads To Specific Down-Regulation Of Itpr3 In Sh-Sy5y Cells
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Stim1 Deficiency Leads To Specific Down-Regulation Of Itpr3 In Sh-Sy5y Cells
Rac1-Dependent Orai1 Translocation To The Leading Edge Supports Lamellipodia Formation And Directional Persistence
Fluctuation In O-Glcnacylation Inactivates Stim1 To Reduce Store-Operated Calcium Ion Entry Via Down-Regulation Of Ser621phosphorylation
Rac1-Dependent Orai1 Translocation To The Leading Edge Supports Lamellipodia Formation And Directional Persistence
Fluctuation In O-Glcnacylation Inactivates Stim1 To Reduce Store-Operated Calcium Ion Entry Via Down-Regulation Of Ser621phosphorylation
Correction To: Stim1 Deficiency Is Linked To Alzheimer’s Disease And Triggers Cell Death In Sh-Sy5y Cells By Upregulation Of L-Type Voltage-Operated Ca2+ Entry (Journal Of Molecular Medicine, (2018), 96, 10, (1061-1079), 10.1007/s00109-018-1677-Y)
Fluctuation In O-Glcnacylation Inactivates Stim1 To Reduce Store-Operated Calcium Ion Entry Via Down-Regulation Of Ser621phosphorylation
Correction To: Stim1 Deficiency Is Linked To Alzheimer’s Disease And Triggers Cell Death In Sh-Sy5y Cells By Upregulation Of L-Type Voltage-Operated Ca2+ Entry (Journal Of Molecular Medicine, (2018), 96, 10, (1061-1079), 10.1007/s00109-018-1677-Y)
Role Of Stim1 In Neurodegeneration
Correction To: Stim1 Deficiency Is Linked To Alzheimer’s Disease And Triggers Cell Death In Sh-Sy5y Cells By Upregulation Of L-Type Voltage-Operated Ca2+ Entry (Journal Of Molecular Medicine, (2018), 96, 10, (1061-1079), 10.1007/s00109-018-1677-Y)
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A Subset Of Orai1α And Orai1β Subunits Heteromerizes To Form Crac Channels
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