MOB1A Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population with targeted disruption of the MOB1A gene. This product consists of a heterogeneous pool of Raji B lymphoblastoid cells in which MOB1A function has been ablated, providing a loss-of-function model for studying Hippo signaling in a B-cell lymphoma context. The polyclonal nature avoids clonal biases and enables reproducible population-level assays.
The Raji cell line is a well-established Epstein-Barr virus (EBV)-positive B lymphoblastoid line derived from a Burkitt lymphoma patient. As a model for B-cell signaling and lymphomagenesis, Raji cells exhibit characteristics of mature B lymphocytes and are widely employed in studies of B-cell malignancies, including lymphoma biology, immune signaling, and tumorigenesis. The EBV-positive status and lymphoblastoid phenotype provide a physiologically relevant context for examining the interplay between viral oncogenesis and cellular tumor suppressor pathways such as Hippo signaling.
MOB1A functions as a kinase activator in the Hippo pathway, where it is phosphorylated by the upstream kinases STK4/MST1 and STK3/MST2. Activated MOB1A binds and stimulates LATS1 and LATS2 kinases, leading to phosphorylation and inactivation of the transcriptional co-activators YAP1 and TAZ/WWTR1. This restricts the expression of proliferative and anti-apoptotic genes such as CTGF and CYR61. MOB1A also interacts with scaffold proteins SAV1 and NF2/Merlin within the Hippo core complex, relaying signals from cell-cell contact and mechanical stress. Disruption of MOB1A thus removes a critical brake on YAP/TAZ-driven oncogenic transcription, highlighting its tumor-suppressive role.
In the context of Burkitt lymphoma-derived Raji cells, MOB1A disruption releases the normal growth-inhibitory constraints imposed by Hippo signaling. Loss of MOB1A prevents the phosphorylation and inactivation of YAP/TAZ, resulting in constitutive nuclear accumulation of YAP1 and unopposed transcriptional activation of CTGF, CYR61, and other oncogenic targets. This promotes enhanced cell proliferation, survival, and potential chemoresistance, mirroring key aspects of aggressive B-cell malignancies. The MOB1A knockout polyclonal Raji model thus provides a powerful tool to dissect the tumor-suppressive role of Hippo signaling in lymphomagenesis and to evaluate therapeutic strategies aimed at restoring YAP/TAZ inhibition.
Applications include mechanistic investigation of Hippo signaling, YAP/TAZ target gene analysis, and functional studies of MOB1A-mediated tumor suppression. Assays such as Western blotting for MOB1A and phospho-YAP, immunofluorescence for YAP localization, RT-qPCR for CTGF and CYR61, and cell proliferation or apoptosis assays are commonly used. This model also supports drug screening for Hippo pathway modulators. For more details, contact Ascent Research.
