Asset Details
Do you wish to reserve the book?
Tcl1 functions as a transcriptional regulator and is directly involved in the pathogenesis of CLL
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.
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?
Tcl1 functions as a transcriptional regulator and is directly involved in the pathogenesis of CLL
Do you wish to request the book?
Tcl1 functions as a transcriptional regulator and is directly involved in the pathogenesis of CLL
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
Tcl1 functions as a transcriptional regulator and is directly involved in the pathogenesis of CLL
2008
Overview
B cell chronic lymphocytic leukemia (B-CLL) is the most common human leukemia. Deregulation of the T cell leukemia/lymphoma 1 (TCL1) oncogene in mouse B cells causes a CD5-positive leukemia similar to aggressive human B-CLLs. To examine the mechanisms by which Tcl1 protein exerts oncogenic activity in B cells, we investigated the effect of Tcl1 expression on NF-κB and activator protein 1 (AP-1) activity. We found that Tcl1 physically interacts with c-Jun, JunB, and c-Fos and inhibits AP-1 transcriptional activity. Additionally, Tcl1 activates NF-κB by physically interacting with p300/CREB binding protein. We then sequenced the TCL1 gene in 600 B-CLL samples and found 2 heterozygous mutations: T38I and R52H. Importantly, both mutants showed gain of function as AP-1 inhibitors. The results indicate that Tcl1 overexpression causes B-CLL by directly enhancing NF-κB activity and inhibiting AP-1.
Publisher
National Academy of Sciences,National Acad Sciences
Subject
/ Animals
/ Chronic lymphocytic leukemia
/ Humans
/ Leukemia
/ Leukemia, Lymphocytic, Chronic, B-Cell - genetics
/ Leukemia, Lymphocytic, Chronic, B-Cell - metabolism
/ Lymphoma
/ Mice
/ mutants
/ Mutation
/ p300-CBP Transcription Factors - metabolism
/ Proteins
/ Proto-Oncogene Proteins - genetics
/ Proto-Oncogene Proteins - metabolism
/ Proto-Oncogene Proteins c-jun - metabolism
/ Rodents
/ Transcription Factor AP-1 - antagonists & inhibitors
/ Transcription Factor AP-1 - genetics
