Evidence That STK19 Is Not an NRAS-dependent Melanoma Driver

Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › fagfællebedømt

Standard

Evidence That STK19 Is Not an NRAS-dependent Melanoma Driver. / Rodríguez-Martínez, Marta; Boissiére, Thierry; Noe Gonzalez, Melvin; Litchfield, Kevin; Mitter, Richard; Walker, Jane; Kjœr, Svend; Ismail, Mohamed; Downward, Julian; Swanton, Charles; Svejstrup, Jesper Q.

I: Cell, Bind 181, Nr. 6, 2020, s. 1395-1405.e11.

Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › fagfællebedømt

Harvard

Rodríguez-Martínez, M, Boissiére, T, Noe Gonzalez, M, Litchfield, K, Mitter, R, Walker, J, Kjœr, S, Ismail, M, Downward, J, Swanton, C & Svejstrup, JQ 2020, 'Evidence That STK19 Is Not an NRAS-dependent Melanoma Driver', Cell, bind 181, nr. 6, s. 1395-1405.e11. https://doi.org/10.1016/j.cell.2020.04.014

APA

Rodríguez-Martínez, M., Boissiére, T., Noe Gonzalez, M., Litchfield, K., Mitter, R., Walker, J., Kjœr, S., Ismail, M., Downward, J., Swanton, C., & Svejstrup, J. Q. (2020). Evidence That STK19 Is Not an NRAS-dependent Melanoma Driver. Cell, 181(6), 1395-1405.e11. https://doi.org/10.1016/j.cell.2020.04.014

Vancouver

Rodríguez-Martínez M, Boissiére T, Noe Gonzalez M, Litchfield K, Mitter R, Walker J o.a. Evidence That STK19 Is Not an NRAS-dependent Melanoma Driver. Cell. 2020;181(6):1395-1405.e11. https://doi.org/10.1016/j.cell.2020.04.014

Author

Rodríguez-Martínez, Marta ; Boissiére, Thierry ; Noe Gonzalez, Melvin ; Litchfield, Kevin ; Mitter, Richard ; Walker, Jane ; Kjœr, Svend ; Ismail, Mohamed ; Downward, Julian ; Swanton, Charles ; Svejstrup, Jesper Q. / Evidence That STK19 Is Not an NRAS-dependent Melanoma Driver. I: Cell. 2020 ; Bind 181, Nr. 6. s. 1395-1405.e11.

Bibtex

@article{a0512394ae6d461d97357f5fbfe41eb8,

title = "Evidence That STK19 Is Not an NRAS-dependent Melanoma Driver",

abstract = "STK19 was proposed to be a cancer driver, and recent work by Yin et al. (2019) in Cell suggested that the frequently recurring STK19 D89N substitution represents a gain-of-function change, allowing increased phosphorylation of NRAS to enhance melanocyte transformation. Here we show that the STK19 gene has been incorrectly annotated, and that the expressed protein is 110 amino acids shorter than indicated by current databases. The {"}cancer driving{"} STK19 D89N substitution is thus outside the coding region. We also fail to detect evidence of the mutation affecting STK19 expression; instead, it is a UV signature mutation, found in the promoter of other genes as well. Furthermore, STK19 is exclusively nuclear and chromatin-associated, while no evidence for it being a kinase was found. The data in this Matters Arising article raise fundamental questions about the recently proposed role for STK19 in melanoma progression via a function as an NRAS kinase, suggested by Yin et al. (2019) in Cell. See also the response by Yin et al. (2020), published in this issue.",

keywords = "GTP Phosphohydrolases/metabolism, Genes, ras, Humans, Melanoma/genetics, Membrane Proteins/genetics, Mutation, Neoplasm Recurrence, Local, Nuclear Proteins, Phosphorylation, Protein-Serine-Threonine Kinases/genetics, Signal Transduction",

author = "Marta Rodr{\'i}guez-Mart{\'i}nez and Thierry Boissi{\'e}re and {Noe Gonzalez}, Melvin and Kevin Litchfield and Richard Mitter and Jane Walker and Svend Kj{\oe}r and Mohamed Ismail and Julian Downward and Charles Swanton and Svejstrup, {Jesper Q}",

year = "2020",

doi = "10.1016/j.cell.2020.04.014",

language = "English",

volume = "181",

pages = "1395--1405.e11",

journal = "Cell",

issn = "0092-8674",

publisher = "Cell Press",

number = "6",

}

RIS

TY - JOUR

T1 - Evidence That STK19 Is Not an NRAS-dependent Melanoma Driver

AU - Rodríguez-Martínez, Marta

AU - Boissiére, Thierry

AU - Noe Gonzalez, Melvin

AU - Litchfield, Kevin

AU - Mitter, Richard

AU - Walker, Jane

AU - Kjœr, Svend

AU - Ismail, Mohamed

AU - Downward, Julian

AU - Swanton, Charles

AU - Svejstrup, Jesper Q

PY - 2020

Y1 - 2020

N2 - STK19 was proposed to be a cancer driver, and recent work by Yin et al. (2019) in Cell suggested that the frequently recurring STK19 D89N substitution represents a gain-of-function change, allowing increased phosphorylation of NRAS to enhance melanocyte transformation. Here we show that the STK19 gene has been incorrectly annotated, and that the expressed protein is 110 amino acids shorter than indicated by current databases. The "cancer driving" STK19 D89N substitution is thus outside the coding region. We also fail to detect evidence of the mutation affecting STK19 expression; instead, it is a UV signature mutation, found in the promoter of other genes as well. Furthermore, STK19 is exclusively nuclear and chromatin-associated, while no evidence for it being a kinase was found. The data in this Matters Arising article raise fundamental questions about the recently proposed role for STK19 in melanoma progression via a function as an NRAS kinase, suggested by Yin et al. (2019) in Cell. See also the response by Yin et al. (2020), published in this issue.

AB - STK19 was proposed to be a cancer driver, and recent work by Yin et al. (2019) in Cell suggested that the frequently recurring STK19 D89N substitution represents a gain-of-function change, allowing increased phosphorylation of NRAS to enhance melanocyte transformation. Here we show that the STK19 gene has been incorrectly annotated, and that the expressed protein is 110 amino acids shorter than indicated by current databases. The "cancer driving" STK19 D89N substitution is thus outside the coding region. We also fail to detect evidence of the mutation affecting STK19 expression; instead, it is a UV signature mutation, found in the promoter of other genes as well. Furthermore, STK19 is exclusively nuclear and chromatin-associated, while no evidence for it being a kinase was found. The data in this Matters Arising article raise fundamental questions about the recently proposed role for STK19 in melanoma progression via a function as an NRAS kinase, suggested by Yin et al. (2019) in Cell. See also the response by Yin et al. (2020), published in this issue.

KW - GTP Phosphohydrolases/metabolism

KW - Genes, ras

KW - Humans

KW - Melanoma/genetics

KW - Membrane Proteins/genetics

KW - Mutation

KW - Neoplasm Recurrence, Local

KW - Nuclear Proteins

KW - Phosphorylation

KW - Protein-Serine-Threonine Kinases/genetics

KW - Signal Transduction

U2 - 10.1016/j.cell.2020.04.014

DO - 10.1016/j.cell.2020.04.014

M3 - Journal article

C2 - 32531245

VL - 181

SP - 1395-1405.e11

JO - Cell

JF - Cell

SN - 0092-8674

IS - 6

ER -

ID: 262752208