Asset Details
MbrlCatalogueTitleDetail
Do you wish to reserve the book?
Oncogenic Potential of the Dual-Function Protein MEX3A
by
Müller, Simon
, Bley, Nadine
, Lederer, Marcell
, Hüttelmaier, Stefan
, Sinz, Andrea
, Glaß, Markus
, Ihling, Christian
in
Cancer
/ Cell cycle
/ Cell migration
/ Cell proliferation
/ Cell self-renewal
/ Gene expression
/ genes
/ Glucose
/ Homology
/ KH domain
/ Localization
/ MEX3A
/ muscles
/ neoplasms
/ oncofetal
/ Post-transcription
/ Post-translation
/ prognosis
/ Proteins
/ Review
/ Ribonucleic acid
/ RING domain
/ RNA
/ RNA binding
/ RNA-binding protein
/ Tumor cells
/ Tumorigenesis
/ Tumors
/ Ubiquitin-protein ligase
/ Ubiquitination
/ Xenografts
/ xenotransplantation
2021
Hey, we have placed the reservation for you!
By the way, why not check out events that you can attend while you pick your title.
You are currently in the queue to collect this book. You will be notified once it is your turn to collect the book.
Oops! Something went wrong.
Looks like we were not able to place the reservation. Kindly try again later.
Are you sure you want to remove the book from the shelf?
Oncogenic Potential of the Dual-Function Protein MEX3A
by
Müller, Simon
, Bley, Nadine
, Lederer, Marcell
, Hüttelmaier, Stefan
, Sinz, Andrea
, Glaß, Markus
, Ihling, Christian
in
Cancer
/ Cell cycle
/ Cell migration
/ Cell proliferation
/ Cell self-renewal
/ Gene expression
/ genes
/ Glucose
/ Homology
/ KH domain
/ Localization
/ MEX3A
/ muscles
/ neoplasms
/ oncofetal
/ Post-transcription
/ Post-translation
/ prognosis
/ Proteins
/ Review
/ Ribonucleic acid
/ RING domain
/ RNA
/ RNA binding
/ RNA-binding protein
/ Tumor cells
/ Tumorigenesis
/ Tumors
/ Ubiquitin-protein ligase
/ Ubiquitination
/ Xenografts
/ xenotransplantation
2021
Oops! Something went wrong.
While trying to remove the title from your shelf something went wrong :( Kindly try again later!
Do you wish to request the book?
Oncogenic Potential of the Dual-Function Protein MEX3A
by
Müller, Simon
, Bley, Nadine
, Lederer, Marcell
, Hüttelmaier, Stefan
, Sinz, Andrea
, Glaß, Markus
, Ihling, Christian
in
Cancer
/ Cell cycle
/ Cell migration
/ Cell proliferation
/ Cell self-renewal
/ Gene expression
/ genes
/ Glucose
/ Homology
/ KH domain
/ Localization
/ MEX3A
/ muscles
/ neoplasms
/ oncofetal
/ Post-transcription
/ Post-translation
/ prognosis
/ Proteins
/ Review
/ Ribonucleic acid
/ RING domain
/ RNA
/ RNA binding
/ RNA-binding protein
/ Tumor cells
/ Tumorigenesis
/ Tumors
/ Ubiquitin-protein ligase
/ Ubiquitination
/ Xenografts
/ xenotransplantation
2021
Please be aware that the book you have requested cannot be checked out. If you would like to checkout this book, you can reserve another copy
We have requested the book for you!
Your request is successful and it will be processed during the Library working hours. Please check the status of your request in My Requests.
Oops! Something went wrong.
Looks like we were not able to place your request. Kindly try again later.
Journal Article
Oncogenic Potential of the Dual-Function Protein MEX3A
2021
Request Book From Autostore
and Choose the Collection Method
Overview
MEX3A belongs to the MEX3 (Muscle EXcess) protein family consisting of four members (MEX3A-D) in humans. Characteristic for MEX3 proteins is their domain structure with 2 HNRNPK homology (KH) domains mediating RNA binding and a C-terminal really interesting new gene (RING) domain that harbors E3 ligase function. In agreement with their domain composition, MEX3 proteins were reported to modulate both RNA fate and protein ubiquitination. MEX3 paralogs exhibit an oncofetal expression pattern, they are severely downregulated postnatally, and re-expression is observed in various malignancies. Enforced expression of MEX3 proteins in various cancers correlates with poor prognosis, emphasizing their oncogenic potential. The latter is supported by MEX3A’s impact on proliferation, self-renewal as well as migration of tumor cells in vitro and tumor growth in xenograft studies.
This website uses cookies to ensure you get the best experience on our website.