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The protein encoded by AMER1 upregulates trancriptional activation by the Wilms tumor protein and interacts with many other proteins, including CTNNB1, APC, AXIN1, and AXIN2. Additionally we are shipping APC Membrane Recruitment Protein 1 Kits (2) and and many more products for this protein.
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Human Polyclonal AMER1 Primary Antibody for FACS, IHC (p) - ABIN390467
Rivera, Kim, Wells, Stone, Burger, Coffman, Zhang, Haber: The tumor suppressor WTX shuttles to the nucleus and modulates WT1 activity. in Proceedings of the National Academy of Sciences of the United States of America 2009
Show all 2 references for ABIN390467
Human Polyclonal AMER1 Primary Antibody for EIA, IHC (p) - ABIN453469
Fukuzawa, Anaka, Weeks, Morison, Reeve: Canonical WNT signalling determines lineage specificity in Wilms tumour. in Oncogene 2009
Show all 2 references for ABIN453469
WTX stabilized chromatin binding by TRIM28 (show TRIM28 Antibodies) and contributed to transcriptional repression of repetitive sequences by TRIM28 (show TRIM28 Antibodies) in mouse embryonic stem cells.
The constellation of anomalies in Wtx null mice suggests that this tumor suppressor broadly regulates mesenchymal progenitor cells in multiple tissues.
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.
Losses of AMER1 by other mechanisms apart from mutations.
A nonsense mutation (c.1045C>T, p.Glu349*) in the WTX gene.
Data show that beta-arrestins regulate Wnt3a (show WNT3A Antibodies)-induced low density lipoprotein receptor-related protein 6 (Lrp6 (show LRP6 Antibodies)) phosphorylation by the regulation of the membrane dynamics of Amer1.
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.
Data indicate that osteopathia striata congenita with cranial sclerosis (OSCS) iscaused by germline deletions of in the X-linked gene WTX (FAM123B, AMER1).
Two novel WTX mutations underscore the unpredictability of male survival in osteopathia striata with cranial sclerosis.
Stat3 (show STAT3 Antibodies) inhibits WTX expression through up-regulation of micro RNA-370 in Wilms tumor.
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.
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.
WTX modulates p53 (show TP53 Antibodies) function, in part through regulation of its activator CBP/p300 (show CREBBP Antibodies).
The protein encoded by this gene upregulates trancriptional activation by the Wilms tumor protein and interacts with many other proteins, including CTNNB1, APC, AXIN1, and AXIN2. Defects in this gene are a cause of osteopathia striata with cranial sclerosis (OSCS).
APC membrane recruitment protein 1
, family with sequence similarity 123, member B
, protein Fam123b
, Wilms tumor gene on the X chromosome protein
, Wilms tumor on the X
, adenomatous polyposis coli membrane recruitment 1
, family with sequence similarity 123B
, protein FAM123B
, APC membrane recruitment 1
, Protein FAM123B