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The mouse homolog of AKTIP produces fused toes and thymic hyperplasia in heterozygous mutant animals while homozygous mutants die in early development. De plus, nous expédions AKTIP Anticorps (77) et AKTIP Protéines (12) et beaucoup plus de produits pour cette protéine.
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Results show that AKTIP co-purifies with A- and B-type lamins and partially co-localizes with lamins in interphase nuclei. In addition, AKTIP depletion lowers lamin A expression and induces senescence hallmarks including telomere homeostasis in human primary fibroblasts.
results suggest that AKT1, FTO, and AKTIP polymorphisms were not associated with obesity/overweight in Brazilians children.
FTS is involved in EGFR-mediated repair of DNA damage induced by cisplatin in ME180 cells
AKTIP interacts with telomeric DNA and is required for telomere maintenance.
High fused toes homolog expression is associated with radioresistance in cervical cancer.
FTS silencing reduced EMT and cell migration by EGF treatment. These results demonstrate a novel function for FTS in EGF-mediated EMT process.
*AKTIP single nucleotide polymorphisms are not associated with late-onset depression patients compared to healthy elderly controls.
Targeted inhibition of FTS led to the shutdown of key elemental characteristics of cervical cancer and could lead to an effective therapeutic strategy.
These data unraveled the involvement of new oncoprotein FTS in cervical cancer which plays a central role in carcinogenesis.
Demographic and clinical characteristics and AKT1 single markers and haplotypes, but not AKTIP polymorphisms or interactions between AKT1 and AKTIP, are associated with increased risk for suicidal behavior in bipolar patients.
Ft1 protein interacts directly with PKB, enhancing the phosphorylation of both of its regulatory sites by promoting its interaction with the upstream kinase PDK1
These data suggest that the FTS/Hook/FHIP complex functions to promote vesicle trafficking and/or fusion via the homotypic vacuolar protein sorting complex.
Ft1 protein is required for telomere maintenance.
Primordial germ cell proliferation is impaired in Fused Toes mutant embryos.
Owing to a deletion, six genes, including the entire IroquoisB (IrxB) gene cluster, are directly affected by the Ft mutation.
Ft genes play an important role in dorsal-ventral patterning of the neural tube acting to define the extent of motor neuron generation
Defects in brain patterning and head morphogenesis are caused by mutations in Fused toes gene.
The mouse homolog of this gene produces fused toes and thymic hyperplasia in heterozygous mutant animals while homozygous mutants die in early development. This gene may play a role in apoptosis as these morphological abnormalities are caused by altered patterns of programmed cell death. The protein encoded by this gene is similar to the ubiquitin ligase domain of other ubiquitin-conjugating enzymes but lacks the conserved cysteine residue that enables those enzymes to conjugate ubiquitin to the target protein. This protein interacts directly with serine/threonine kinase protein kinase B (PKB)/Akt and modulates PKB activity by enhancing the phosphorylation of PKB's regulatory sites. Alternative splicing results in two transcript variants encoding the same protein.
AKT interacting protein
, fused toes homolog
, AKT-interacting protein
, Fused toes protein homolog
, fused toes protein homolog
, AKT-interacting protein homolog B
, fused toes protein