The DEGS1 Knockout Raji Polyclonal Cells product offers a heterogeneous population of Raji B lymphocytes with CRISPR/Cas9-mediated disruption of the DEGS1 gene, serving as a model for sphingolipid metabolism and ceramide signaling studies. This polyclonal knockout system provides a genetically defined loss-of-function approach without pharmacological inhibitors.
Raji cells, derived from a Burkitt??s lymphoma patient, are human B lymphocytes that grow in suspension and exhibit surface immunoglobulin expression, antibody production, and antigen presentation. They are extensively used to study B cell receptor (BCR) signaling, lymphomagenesis, and immune cell biology.
DEGS1 (delta-4-desaturase, sphingolipid) introduces a double bond into dihydroceramide to produce ceramide, a pivotal sphingolipid mediating apoptosis, proliferation, and stress responses. Its expression is regulated by the transcription factor SP1 in response to cellular stress and sphingolipid intermediates. Ceramide acts through downstream targets such as protein phosphatase 2A (PP2A), protein kinase C zeta (PKC??), and caspases, integrating signals from dihydroceramide and ceramide synthases. Disruption of DEGS1 leads to dihydroceramide accumulation and ceramide depletion, perturbing sphingolipid network homeostasis.
In the Raji B lymphocyte, DEGS1 knockout disrupts ceramide balance, potentially altering BCR signaling and apoptotic threshold. Ceramide promotes apoptosis in lymphoma cells, so its reduction may favor survival, while dihydroceramide accumulation might cause independent effects. This model aids in studying how sphingolipid dysregulation affects lymphoma cell fate, autophagy, and drug sensitivity, with relevance to cancer and hypomyelinating leukodystrophy.
Applications include sphingolipid profiling via mass spectrometry, western blotting of ceramide targets, apoptosis flow cytometry, BCR phospho-signaling assays, and proliferation studies under drug treatments. These cells facilitate research into ceramide??s role in B cell lymphoma biology and therapy resistance. For detailed inquiries, please contact Ascent Research.
