anti-TBC1 Domain Family, Member 3 (TBC1D3) Antibodies

Human TBC1 Domain Family, Member 3 (TBC1D3) interaction partners

1. our work reveals a novel model by which CaM promotes cell migration through inhibiting the ubiquitination and degradation of TBC1D3.

2. Here, the found that expression of TBC1D3 in ventricular cortical progenitors of mice via in utero electroporation caused delamination of ventricular radial glia cells (vRGs) and promoted generation of self-renewing basal progenitors with typical morphology of outer radial glia (oRG), which are most abundant in primates. Expression of TBC1D3, was often found to underlie cortical regions exhibiting folding.

3. these studies indicate a novel model by which the microtubule network regulates EGFR (show EGFR Antibodies) stability and signaling through tubulin (show TUBB Antibodies) dimer/oligomer interaction with the nucleocytoplasmic protein TBC1D3.

4. TBC1D3 is targeted to the plasma membrane by protein palmitoylation.

5. Growth factor-stimulated TBC1D3 ubiquitination and degradation are regulated by its interaction with CUL7 (show CUL7 Antibodies)-Fbw8 (show FBXW8 Antibodies).

6. TBC1D3 plays an unanticipated and potentially unique role in the fine-tuning of insulin (show INS Antibodies)/IGF-1 (show IGF1 Antibodies) signaling

7. We describe eight highly related TBC1D3 paralogues located on Chromosome 17q12 that display specific transcription patterns in human tissues, and that pattern is altered in several primary prostate tumors in comparison to healthy prostate tissues.

8. Altered growth factor receptor (show RYK Antibodies) trafficking and GTP (show AK3 Antibodies)-Ras turnover may be sites where recently evolved genes such as TBC1D3 selectively modulate signaling in hominoids and humans