SH3-Domain Binding Protein 5 (BTK-Associated) Proteins (SH3BP5)

Human SH3-Domain Binding Protein 5 (BTK-Associated) (SH3BP5) interaction partners

1. SH3BP5, LMO3, and SNAP25 were expressed in diffuse large B-cell lymphoma cells and associated with clinical features.

2. REI/SH3BP5 protein family is conserved in evolution and is a group of new guanine nucleotide exchange factors for Rab11.

3. The interplay of p-JNK with mitochondrial Sab leads to impaired respiration, ROS production, sustained JNK activation, and apoptosis.

4. SH3BP5 binds to JNK and directly inhibits JNK through its two putative mitogen-activated protein kinase interaction motifs (KIMs).

5. mitochondrial protein Sab is phosphorylated by stress-activated protein kinase 3

Mouse (Murine) SH3-Domain Binding Protein 5 (BTK-Associated) (SH3BP5) interaction partners

1. 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.

2. The interplay of p-JNK with mitochondrial Sab leads to impaired respiration, ROS production, sustained JNK activation, and apoptosis.

3. ER stress triggers an interaction of JNK with mitochondrial Sab, which leads to impaired respiration and increased mitochondrial reactive oxygen species.

4. SH3BP5 binds to JNK and directly inhibits JNK through its two putative mitogen-activated protein kinase interaction motifs (KIMs).

5. JNK-dependent acute liver injury from acetaminophen or tumor necrosis factor (TNF) requires mitochondrial Sab protein expression in mice