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May function in the regulation of planar cell polarity.
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Study shows that when key regulators during mammalian cerebral cortical development are disrupted due to DCHS1 (show DCHS1 Antibodies)-FAT4 mutations, functional cerebral asymmetries are stronger.
Epigenetic inactivation of FAT4 contributes to gastric field cancerization.
In hepatocellular carcinoma patients, both FAT4 expression and FAT4 mutational status significantly correlated with patient prognosis. FAT4 acts as a putative tumor suppressor that is frequently inactivated in human hepatocellular carcinoma.
In conclusion, Fat4 expression is deceased in gastric cancer cells, leading to nuclear translocation of Yap (show YAP1 Antibodies) and correlates with poor prognosis.
FAT4 has a tumour suppressor role mediated by the modulation of Wnt (show WNT2 Antibodies)/beta-catenin (show CTNNB1 Antibodies) signalling, providing potential novel targets for the treatment of gastric cancer
our results reveal a novel inhibitory mechanism of FAT4 gene expression through actin depolymerization during Src (show SRC Antibodies)-induced carcinogenesis in human breast cells.
These findings suggest that Fat and Dachsous self-bend due to the loss of Ca(2 (show CA2 Antibodies)+)-binding amino acids from specific EC-EC (show QPCT Antibodies) linkers, and can therefore adapt to confined spaces.
study defined eight additional recurrently mutated genes in SMZL; these genes are CREBBP (show CREBBP Antibodies), CBFA2T3 (show CBFA2T3 Antibodies), AMOTL1 (show AMOTL1 Antibodies), FAT4, FBXO11 (show FBXO11 Antibodies), PLA2G4D, TRRAP (show TRRAP Antibodies) and USH2A (show USH2A Antibodies).
Homozygosity mapping and whole-exome sequencing was used in the original Hennekam syndrome family with multiple affected individuals in whom no CCBE1 (show CCBE1 Antibodies) mutation had been detected, and identified a homozygous mutation in the FAT4 gene.
findings show that mutations in genes encoding the receptor-ligand cadherin pair DCHS1 (show DCHS1 Antibodies) and FAT4 lead to a recessive syndrome in humans that includes periventricular neuronal heterotopia
Fat4 and Dachsous1 are critical regulators of lymphatic valve morphogenesis. Valve defects may contribute to lymphedema in Hennekam syndrome caused by Fat4 mutations.
novel mechanisms of Fat4-Dchs1 (show DCHS1 Antibodies) signalling have evolved to control cell proliferation within the developing vertebrae.
Fat1 (show FAT1 Antibodies) interacts with Fat4 to regulate neural tube closure, neural progenitor proliferation and apical constriction during mouse brain development.
Stromal Fat4 acts non-autonomously with Dchs1 (show DCHS1 Antibodies)/2 to restrict the nephron progenitor pool.
Fat4/Dchs1 (show DCHS1 Antibodies) signaling between stromal and cap mesenchyme cells influences nephrogenesis and ureteric bud branching.
Data find that Fat1 (show FAT1 Antibodies) and Fat4 cooperate during mouse development to control renal tubular elongation, cochlear extension, cranial neural tube formation and patterning of outer hair cells in the cochlea.
Fat4 and Tsc22d1 (show TSC22D1 Antibodies) are likely candidate genes to influence formation of spontaneous pulmonary adenoma in aging male and female mice, respectively.
Dchs1 (show DCHS1 Antibodies) and Fat4 function as a ligand-receptor pair during murine development, and novel requirements for Dchs1 (show DCHS1 Antibodies)-Fat4
Study shows that Fat4 is an essential gene that has a key role in vertebrate core planar cell polarity; loss of Fat4 disrupts oriented cell divisions and tubule elongation during kidney development, leading to cystic kidney disease.
May function in the regulation of planar cell polarity. Cadherins are cell-cell interaction molecules (By similarity).
FAT tumor suppressor homolog 4
, cadherin family member 14
, cadherin-related family member 11
, fat-like cadherin FATJ
, fat-like cadherin protein FAT-J
, protocadherin Fat 4
, putative protein product of Nbla00548