MAX Dimerization Protein 1 (MXD1) ELISA Kits

Human MAX Dimerization Protein 1 (MXD1) interaction partners

1. these data show that MXD1 functions as a negative regulator of BCR-ABL1 expression and subsequently inhibits proliferation and sensitizes chronic myeloid leukemia cells to imatinib treatment

2. Results suggest a role for MAX dimerization protein 1 (MXD1) in the control of ribosome biogenesis.

3. Study revealed that HIF-1alpha-induced Mxd1 contributes to cisplatin-resistance in hypoxic osteosarcoma cells by directly repressing PTEN, which leads to the activation of PI3K/AKT antiapoptotic and survival pathway.

4. the miR-382-5p/MXD1 axis plays a critical role in myelopoiesis by affecting the lineage choice of CD34(+) hematopoietic stem/progenitor cells.

5. TCP10L stabilizes MAD1 protein level through direct interaction, and they cooperatively regulate cell cycle progression.

6. down regulation of miR-202 increased the expression of its target Mxd1, followed by Mxd1 recruitment to the Sin3A repressor complex and through its dimerization with Max, and increased repression of Myc-Max target proteins.

7. miR-17-92 cluster members miR-19a/b facilitated gastric cancer cell migration, invasion and metastasis through targeting the antagonist of c-Myc -- MXD1.

8. This study suggests that genetic variants of MXD1 may modulate the effect of smoking on carotid plaque burden.

9. Mad1 gene transfer inhibits the proliferation of human melanoma cells

10. HBP1 and Mad1 repressors bind the Sin3 corepressor PAH2 domain with opposite helical orientations

11. MAD1 and Proto-Oncogene Proteins c-myc reciprocally regulate ribosomal DNA transcription, providing a mechanism for coordination of ribosome biogenesis and cell growth

12. c-myc and mad1 can regulate the hTERT transcript in a different manner in hTERT positive cells, but not in normal cells

13. Mad1, Mxi1 and Rox genes were expressed and displayed mutations in haematological malignancies.

14. This study provides a direct link between the growth factor signaling pathways regulated by PI3 kinase/Akt and MAP kinases with Myc-mediated transcription.

15. TGF-beta can override Myc activity despite a stabilizing cancer mutation and induce senescence in myeloid tumor cells, at least in part by induction of Mad1

16. examination of functionality of basic domains compared with Myc

17. X-ray structures of Myc-Max and Mad-Max recognizing DNA. Molecular bases of regulation by proto-oncogenic transcription factors.

18. Mad expression and Id2 down-regulation are important events during the TGF-beta cytostatic program in epithelial cells.

19. Max as a novel co-activator of C/EBPalpha functions, thereby suggesting a possible link between C/EBPalpha and Myc-Max-Mad network.

20. The PTEN tumor suppressor gene is a target of MAD1.

Mouse (Murine) MAX Dimerization Protein 1 (MXD1) interaction partners

1. 1,25D and the VDR regulate the c-MYC/MXD1 network to suppress c-MYC function, providing a molecular basis for cancer preventive actions of vitamin D.

2. Phe-7 is the critical determinant and provides the molecular specificity for the association between Sin3 and Mad in regulating cell growth and differentiation.

3. Mad1 is a transcriptional repressor of Bcl-6.