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May function in the regulation of planar cell polarity.
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The results provide direct evidence that localized feedbacks on Fat4-Ds1 (zeige ICT1 Antikörper) complexes can give rise to planar cell polarity.
Study shows that when key regulators during mammalian cerebral cortical development are disrupted due to DCHS1 (zeige DCHS1 Antikörper)-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 (zeige YAP1 Antikörper) and correlates with poor prognosis.
FAT4 has a tumour suppressor role mediated by the modulation of Wnt (zeige WNT2 Antikörper)/beta-catenin (zeige CTNNB1 Antikörper) 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 (zeige SRC Antikörper)-induced carcinogenesis in human breast cells.
These findings suggest that Fat and Dachsous self-bend due to the loss of Ca(2 (zeige CA2 Antikörper)+)-binding amino acids from specific EC-EC (zeige QPCT Antikörper) linkers, and can therefore adapt to confined spaces.
study defined eight additional recurrently mutated genes in SMZL; these genes are CREBBP (zeige CREBBP Antikörper), CBFA2T3 (zeige CBFA2T3 Antikörper), AMOTL1 (zeige AMOTL1 Antikörper), FAT4, FBXO11 (zeige FBXO11 Antikörper), PLA2G4D (zeige PLA2G4D Antikörper), TRRAP (zeige TRRAP Antikörper) and USH2A (zeige USH2A Antikörper).
Homozygosity mapping and whole-exome sequencing was used in the original Hennekam syndrome family with multiple affected individuals in whom no CCBE1 (zeige CCBE1 Antikörper) mutation had been detected, and identified a homozygous mutation in the FAT4 gene.
Dchs1 (zeige DCHS1 Antikörper)-Fat4 planar cell polarity pathway controls cell orientation in the early skeletal condensation to define the shape and relative dimensions of the mouse sternum.
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 (zeige DCHS1 Antikörper) signalling have evolved to control cell proliferation within the developing vertebrae.
Fat1 (zeige FAT1 Antikörper) 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 (zeige DCHS1 Antikörper)/2 to restrict the nephron progenitor pool.
Fat4/Dchs1 (zeige DCHS1 Antikörper) signaling between stromal and cap mesenchyme cells influences nephrogenesis and ureteric bud branching.
Data find that Fat1 (zeige FAT1 Antikörper) 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 (zeige TSC22D1 Antikörper) are likely candidate genes to influence formation of spontaneous pulmonary adenoma in aging male and female mice, respectively.
Dchs1 (zeige DCHS1 Antikörper) and Fat4 function as a ligand-receptor pair during murine development, and novel requirements for Dchs1 (zeige DCHS1 Antikörper)-Fat4
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