anti-APC Membrane Recruitment Protein 1 (AMER1) Antibodies

Mouse (Murine) APC Membrane Recruitment Protein 1 (AMER1) interaction partners

1. analysis provides a novel model for WTX-caused bone diseases and explains on the molecular level how truncation mutations in this gene may retain some of WTX-protein functions.

2. WTX stabilized chromatin binding by TRIM28 and contributed to transcriptional repression of repetitive sequences by TRIM28 in mouse embryonic stem cells.

3. The constellation of anomalies in Wtx null mice suggests that this tumor suppressor broadly regulates mesenchymal progenitor cells in multiple tissues.

4. The observed phenotypic discordance dependent upon whether a mutation is germline or occurs somatically suggests the existence of temporal or spatial constraints on the action of WTX during tumorigenesis.

Human APC Membrane Recruitment Protein 1 (AMER1) interaction partners

1. This study revealed no clinical or pathologic distinctions between Wilms tumor (WT) with and without WTX mutation. This similarity lends support to the concept of a common tumorigenic pathway between WT with aberrant WTX and those without.

2. Data suggest that the aberrant upregulation of miR-20a/miR-106a as the reason of Wilms tumor gene on the X chromosome (WTX) loss in colorectal cancer (CRC) both in vivo and in vitro.

3. A novel heterozygous frameshift mutation in AMER1 was identified in a patient with osteopathia striata with cranial sclerosis.

4. Losses of AMER1 by other mechanisms apart from mutations.

5. A nonsense mutation (c.1045C>T, p.Glu349*) in the WTX gene.

6. Data show that beta-arrestins regulate Wnt3a-induced low density lipoprotein receptor-related protein 6 (Lrp6) phosphorylation by the regulation of the membrane dynamics of Amer1.

7. WTX inactivation occurs in a wider variety of tumor types than previously appreciated and point to shared pathogenic mechanisms between a subset of pediatric malignancies.

8. Data indicate that osteopathia striata congenita with cranial sclerosis (OSCS) iscaused by germline deletions of in the X-linked gene WTX (FAM123B, AMER1).

9. Two novel WTX mutations underscore the unpredictability of male survival in osteopathia striata with cranial sclerosis.

10. Stat3 inhibits WTX expression through up-regulation of micro RNA-370 in Wilms tumor.

11. Osteopathia striata with cranial sclerosis or Horan-Beighton syndrome is a rare X-linked dominant inherited bone dysplasia. Genetic analysis allowed the identification of maternally transmitted heterozygous nonsense c.1057C>T (p.R353X) WTX mutation.

12. WTX mutations occur early in Wilms' tumor development, but at a low proportion. There was no evidence that WTX is the main cause of Wilms' tumor.

13. WTX modulates p53 function, in part through regulation of its activator CBP/p300.

14. WTX and NRF2 compete for binding to KEAP1, and thus loss of WTX leads to rapid ubiquitination and degradation of NRF2 and a reduced response to cytotoxic insult.

15. Amer1 exerts its negative regulatory role in Wnt signaling by acting as a scaffold protein for the beta-catenin destruction complex and promoting stabilization of Axin at the plasma membrane.

16. WTX mutations can arise both early and late in Wilms tumour development

17. When gene expression changes mediated by wild-type WTX were compared with those affected by mutant WTX, WTX565 had a 55% overlap in differentially regulated genes, whereas WTX358 regulated only two genes affected by wild-type WTX.

18. Mutations in the WTX-gene are associated with high-grade microsatellite instable colorectal cancers.

19. inactivation of WTX appears to be a late event in tumorigenesis of nephroblastoma in a subgroup of nephroblastomas

20. All investigated families diagnosed with Osteopathia striata with cranial sclerosis had WTX gene defects.