Zobrazeno 1 - 8
of 8
pro vyhledávání: '"Joshua A Molina"'
Publikováno v:
mBio, Vol 13, Iss 3 (2022)
ABSTRACT Decapping enzymes remove the 5′ cap of eukaryotic mRNA, leading to accelerated RNA decay. They are critical in regulating RNA homeostasis and play essential roles in many cellular and life processes. They are encoded in many organisms and
Externí odkaz:
https://doaj.org/article/35729c16721a4d859e13724eb116b64e
Autor:
Joshua A. Molina, Zhilong Yang
Publikováno v:
Journal of Medical Virology. 94:3811-3819
Host shutoff, characterized by a global decline of cellular protein synthesis, is commonly observed in many viral infections, including vaccinia virus (VACV). Classic methods measuring host shutoff include the use of radioactive or nonradioactive pro
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::24b90bb82f1ac03a5f3329534be5e711
https://doi.org/10.1002/jmv.27773
https://doi.org/10.1002/jmv.27773
Publikováno v:
Pathogens, Vol 9, Iss 5, p 400 (2020)
The synthesis of host cell proteins is adversely inhibited in many virus infections, whereas viral proteins are efficiently synthesized. This phenomenon leads to the accumulation of viral proteins concurrently with a profound decline in global host p
Externí odkaz:
https://doaj.org/article/894edfef40454597be5864673df746b8
Decapping enzymes remove the 5’-cap of eukaryotic mRNA, leading to accelerated RNA decay. They are critical in regulating RNA homeostasis and play essential roles in many cellular and life processes. They are encoded in many organisms and viruses,
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::7390c9d0028f89619e0134bd7e9b0a97
https://doi.org/10.1101/2021.10.22.465448
https://doi.org/10.1101/2021.10.22.465448
Publikováno v:
Pathogens
Pathogens, Vol 9, Iss 400, p 400 (2020)
Pathogens, Vol 9, Iss 400, p 400 (2020)
The synthesis of host cell proteins is adversely inhibited in many virus infections, whereas viral proteins are efficiently synthesized. This phenomenon leads to the accumulation of viral proteins concurrently with a profound decline in global host p
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::d905bc85eb807f47aad35dd722d5c92f
https://pubmed.ncbi.nlm.nih.gov/32455727
https://pubmed.ncbi.nlm.nih.gov/32455727
Publikováno v:
Biochimica et Biophysica Acta (BBA) - Molecular Cell Research. 1865:1356-1367
Lysosomes are a major organelle for degrading macromolecules. When deprived of nutrients, cells activate the autophagy and lysosome biogenesis pathways to recycle cytoplasmic materials and to increase lysosomal degradation capacity for survival, resp
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::e70ecf68a3e382b0600635f38a34af4b
https://doi.org/10.1016/j.bbamcr.2018.06.014
https://doi.org/10.1016/j.bbamcr.2018.06.014
Autor:
Melissa Feuerborn, Alexa R. Wilden, Joshua A. Molina, Stella Y. Lee, Jessie Adams, Theodore Budden, Babita Adhikari
Publikováno v:
Scientific Reports
Scientific Reports, Vol 9, Iss 1, Pp 1-12 (2019)
Scientific Reports, Vol 9, Iss 1, Pp 1-12 (2019)
Neuronal ceroid lipofuscinoses (NCLs) are a group of inherited neurodegenerative lysosomal storage disorders. CLN5 deficiency causes a subtype of NCL, referred to as CLN5 disease. CLN5 is a soluble lysosomal protein with an unclear function in the ce
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::50465d47ffb7bf46031486a143abea3d
https://doi.org/10.1038/s41598-018-36379-z
https://doi.org/10.1038/s41598-018-36379-z
Publikováno v:
Biochimica et biophysica acta. Molecular basis of disease. 1865(2)
The neuronal ceroid lipofuscinoses (NCLs) are a group of inherited neurodegenerative lysosomal storage disorders. CLN8 deficiency causes a subtype of NCL, referred to as CLN8 disease. CLN8 is an ER resident protein with unknown function; however, a r
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::ef23e8bec0a94b0df9b2decf13e76deb
https://pubmed.ncbi.nlm.nih.gov/30453012
https://pubmed.ncbi.nlm.nih.gov/30453012