14-3-3 beta Protein, Human (GST)

14-3-3 beta protein, functioning as an adapter, regulates diverse signaling pathways by recognizing phosphoserine or phosphothreonine motifs and modulating partner activity. It acts as a negative regulator in osteogenesis, inhibiting SRPK2's nuclear translocation and preventing neuronal apoptosis. Additionally, it negatively regulates MAP kinase-activating cascades through AKAP13. As a homodimer, it interacts with various proteins, emphasizing its diverse roles in cellular processes and signaling pathways. 14-3-3 beta Protein, Human (GST) is the recombinant human-derived 14-3-3 beta protein, expressed by E. coli, with N-GST labeled tag. The total length of 14-3-3 beta Protein, Human (GST) is 246 a.a., with molecular weight of ~52 kDa.

The 14-3-3 beta protein serves as an adapter implicated in the regulation of a wide spectrum of both general and specialized signaling pathways. Recognizing phosphoserine or phosphothreonine motifs, it binds to numerous partners, modulating the activity of the binding partner upon interaction. It acts as a negative regulator of osteogenesis by blocking the nuclear translocation of the phosphorylated form of SRPK2, counteracting its stimulatory effect on cyclin D1 expression, and thereby preventing neuronal apoptosis induced by SRPK2. Additionally, 14-3-3 beta negatively regulates signaling cascades that activate MAP kinases through AKAP13. Existing as a homodimer, it interacts with various proteins, including SAMSN1, PRKCE, AKAP13, SSH1, TORC2/CRTC2, ABL1, ROR2, GAB2, YAP1, SRPK2, PKA-phosphorylated AANAT, MYO1C, SIRT2, DAPK2, PI4KB, TBC1D22A, TBC1D22B, SOS1, YWHAB, SLITRK1, SYNPO2, RIPOR2, MARK2, MARK3, TESK1, MEFV, HDAC4, and ADAM22. These interactions highlight the diverse roles of 14-3-3 beta in various cellular processes and signaling pathways.

Human

E. coli

N-GST

P31946 (M1-N246)

7529  [NCBI]

Approximately 52 kDa

Greater than 95% as determined by reducing SDS-PAGE.

<1 EU/μg, determined by LAL method.