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may bind c-Jun N-terminal kinase (JNK)\; may play a role in JNK and Bruton's tyrosine kinase (Btk) mediated signaling pathways [RGD, Feb 2006].. Additionally we are shipping SH3-Domain Binding Protein 5 (BTK-Associated) Antibodies (28) and SH3-Domain Binding Protein 5 (BTK-Associated) Kits (6) and many more products for this protein.
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SH3 domain binding protein 5 (Sab) expression is reduced in ovarian cancer (OC), suggesting that Sab may be a prognostic biomarker to discern personalized treatments for OC patients.
SH3BP5, LMO3, and SNAP25 were expressed in diffuse large B-cell lymphoma cells and associated with clinical features.
REI/SH3BP5 protein family is conserved in evolution and is a group of new guanine nucleotide exchange factors for Rab11.
The interplay of p-JNK with mitochondrial Sab leads to impaired respiration, ROS production, sustained JNK activation, and apoptosis.
SH3BP5 binds to JNK and directly inhibits JNK through its two putative mitogen-activated protein kinase interaction motifs (KIMs).
mitochondrial protein Sab is phosphorylated by stress-activated protein kinase 3
The binding to and phosphorylation of Sab by p-JNK on the outer mitochondrial membrane leads to SHP1-dependent and DOK4-dependent inactivation of p-Src on the inner membrane; inactivation of mitochondrial Src inhibits electron transport and increases reactive oxygen species release, which sustains JNK activation and promotes cell death and organ injury.
ER stress triggers an interaction of JNK with mitochondrial Sab, which leads to impaired respiration and increased mitochondrial reactive oxygen species.
JNK-dependent acute liver injury from acetaminophen or tumor necrosis factor (TNF) requires mitochondrial Sab protein expression in mice
may bind c-Jun N-terminal kinase (JNK)\; may play a role in JNK and Bruton's tyrosine kinase (Btk) mediated signaling pathways
SH3 domain-binding protein 5
, SH3 domain-binding protein that preferentially associates with BTK
, vascular endothelial cell-specific protein 18