Anti-CBL (phospho Y731) antibody [EP973Y] - BSA and Azide free

Supplementary info

This supplementary information is collated from multiple sources and compiled automatically.

Activity summary

The CBL protein also known as C-cbl or Casitas B-lineage lymphoma proto-oncogene serves as an E3 ubiquitin-protein ligase. This protein with a molecular mass of approximately 120-130 kDa plays a critical role in the regulation of receptor tyrosine kinases. It facilitates the polyubiquitination of activated receptor proteins targeting them for degradation in the proteasome. CBL is predominantly expressed in various tissues including the hematopoietic system. It is a significant component in the control of cell signaling and helps maintain cellular homeostasis.

Biological function summary

The CBL protein acts as a negative regulator for several signaling pathways. It integrates into signaling complexes and modulates the activation of pathways by interacting with other proteins. CBL does not act alone; it commonly forms complexes with proteins such as Grb2 and p85 influencing downstream signaling influence in pathways. This regulation prevents excessive activation of signals that can lead to cellular proliferation or differentiation abnormally.

Pathways

CBL integrates into the ubiquitin-proteasome system and the Ras signaling pathway. Within these pathways CBL works to modulate cell surface receptors ensuring that signaling threshold is not surpassed. The importance of CBL in the Ras signaling pathway is highlighted by its interactions with proteins like Ras-GAP and SHP2. Through these interactions CBL controls the rate of signal transduction affecting cellular responses such as growth survival and motility.

Associated diseases and disorders

CBL involvement has been linked to several forms of cancer and immune deficiencies. Mutations or dysregulation of the CBL gene can lead to myelodysplastic syndromes and acute myeloid leukemia. In these conditions the interaction between CBL and other proteins such as JAK2 becomes dysregulated driving abnormal cell growth and survival. Furthermore CBL’s failure to properly degrade tyrosine kinase receptors can contribute to enhanced signaling fostering oncogenic processes.