Browse our anti-BTRC (BTRC) Antibodies

Xenopus laevis beta-Transducin Repeat Containing (BTRC) interaction partners

1. Promoter elements of positive and negative transcriptional control were identified.

2. Strong ERK activation can target Cdc25A for degradation in a manner similar to, but independent of, Chk1 for cell cycle arrest.

Human beta-Transducin Repeat Containing (BTRC) interaction partners

1. Reciprocal regulation between betaTrCP and Smurf1 has been found to inhibit proliferative capacity of liver cancer cells.

2. a phosphorylation mutant form of Mxi1 (Mxi1-S160A), which cannot be degraded by S6K1 and beta-Trcp, is much more stable and efficient in suppressing the transcriptional activity of Myc and radioresistance in lung cancer cells.

3. beta-TrCP was identified as a novel interacting partner of ASK1 that is capable of ubiquitinating and degrading ASK1 through the ubiquitin-proteasome system. These findings suggest that beta-TrCP is capable of suppressing oxidative stress-induced caspase 3-dependent apoptosis through suppression of ASK1.

4. The primary role of the S(52,56) residues of Vpu in antagonism of CD4, GaLV Env, and BST-2/tetherin is to recruit the SCF/betaTrCP ubiquitin ligase.

5. TSPAN15 interacts with BTRC to promote oesophageal squamous cell carcinoma metastasis via activating NF-kappaB signaling.

6. BTrCP-FBXW2-SKP2 axis forms an oncogene-tumour suppressor-oncogene cascade to control cancer cell growth with FBXW2 acting as a tumour suppressor by promoting SKP2 degradation.

7. Data show that the SCF(beta-TrCP) ubiquitin E3 ligase complex responsible for regulating the active protein kinase C-associated kinase (RIPK4) level.

8. SAG/RBX2 E3 ligase complexes with UBCH10 and UBE2S ubiquitin-conjugating enzymes to ubiquitylate beta-TrCP1 via K11-linkage for degradation.

9. Data indicate the role of tyrosine kinase c-Src (Src) in rescuing Taz (transcriptional coactivator with PDZ-binding motif) from E3 ligase SCF(beta-TrCP)-mediated degradation.

10. SCFbeta-TRCP negatively regulates the FLCN complex by promoting FNIP2 degradation in Birt-Hogg-Dube syndrome-associated renal cancer.

11. beta-TRCP depletion in HepG2 hepatocellular carcinoma cells resulted in increased Lipin1 protein abundance.

12. It demonstrates that degradation of Lipin-1 is regulated by BTRC in the cytoplasm and on membranes

13. we identified two independent SNPs (i.e., WNT2B rs1175649 G>T and BTRC rs61873997 G>A) that showed a predictive role in CM-specific survival, with an effect-allele-attributed hazards ratio (adjusted hazards ratio) of 1.99 (95% confidence interval = 1.41-2.81, P = 8.10 x 10(-5)) and 0.61 (0.46-0.80, 3.12x10(-4)), respectively.

14. It has been proposed that CENP-W may function as a booster of beta-TrCP1 nuclear import to increase the oncogenicity of beta-TrCP1.

15. oncogenic effect of miR-182 and its reversal by beta-TrCP2 were confirmed in vivo This study suggests that beta-TrCP and miR-182 may be possible biomarkers and targets for early detection and treatment of pancreatic cancer

16. Beta-TrCP controls ubiquitination and degradation of liver-enriched transcription factor CREB-H.

17. Phosphorylated VEGFR-2 was reduced by hyperglycemia while total VEGFR-2 was almost unaltered. However, VEGFR-2 was reduced when directly exposed to reactive oxygen species, with resultant co-location of beta-TrCP and VEGFR-2.

18. Low GAS7C increases cancer cell motility by promoting N-WASP/FAK/F-actin cytoskeleton dynamics. It also enhances beta-catenin stability via hnRNP U/beta-TrCP complex formation.

19. EBV-miR-BART10-3p facilitated epithelial-mesenchymal transition and promotes metastasis of nasopharyngeal carcinoma by targeting BTRC.

20. beta-TrCP1/FWD1 dominant negative mutant has a role in reducing myeloma cell growth

Mouse (Murine) beta-Transducin Repeat Containing (BTRC) interaction partners

1. beta-TrCP was identified as a novel interacting partner of ASK1 that is capable of ubiquitinating and degrading ASK1 through the ubiquitin-proteasome system. These findings suggest that beta-TrCP is capable of suppressing oxidative stress-induced caspase 3-dependent apoptosis through suppression of ASK1.

2. beta-TrCP regulates the transition from mitosis to meiosis in male germ cells by targeting DMRT1 for degradation.

3. Data indicate a critical physiological function of beta-TRCP in regulating hepatic lipid metabolic homeostasis in part through modulating Lipin1 stability.

4. betaTrCP levels are correlated with imiquimod-induced skin lesion.

5. beta-TrCP1/FWD1 dominant negative mutant has a role in reducing myeloma cell growth

6. Erbin as a novel substrate of SAG-betaTrCP E3 ligase.

7. these results clearly suggest that both beta-TrCP- and Hrd1-dependent degradation mechanisms regulate the transcriptional activity of Nrf1 to maintain cellular homeostasis.

8. beta-TrCP may be an essential player in UVB induced responses in skin

9. Glycogen synthase kinase 3 phosphorylates a group of Ser residues in the Neh6 domain of mouse Nrf2 that overlap with an SCF/beta-TrCP destruction motif (DSGIS, residues 334 to 338) and promotes its degradation in a Keap1-independent manner.

10. LPS appears to destabilize the LPCAT1 protein by GSK-3beta-mediated phosphorylation within a canonical phosphodegron for beta-TrCP docking and site-specific ubiquitination.

11. the two beta-TrCP paralogs have a nonredundant role in spermatogenesis

12. anti-inflammatory effects of H(2)O(2) may result from its ability to decrease ubiquitination as well as subsequent degradation of I kappaB alpha through inhibiting the association between I kappaB alpha and SCF(beta-TrCP)

13. BMP-2 modulates beta-catenin signaling through stimulation of Lrp5 expression and inhibition of beta-TrCP expression in osteoblasts

14. Results suggest a role for Btrc in regulating the eventual ratio of resulting differentiated retinal cell types.

15. hnRNP-U engages a highly neddylated active SCF beta-TrCP which dissociates in the presence of a high-affinity substrate, resulting in the ubiquitination of the latter.

16. HOS plays a role in inhibiting cell differentiation and cell transformation

17. b-TrCP controls meiotic and mitotic progression in vivo.

18. beta-TrCP1 contributes to, but is not absolutely required for, the degradation of I kappa B and beta-catenin

19. mammary glands of betaTrcp1(-/-) female mice display a hypoplastic phenotype, whereas no effects on cell proliferation are observed in other somatic cells

20. Cancer cell lines harboring Smad4 point mutations exhibited rapid Smad4 protein degradation due to the effect of SCF(beta-TrCP1), also called Btrc.