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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. Additionally we are shipping AKTIP Antibodies (77) and AKTIP Proteins (12) and many more products for this protein.
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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 (show LMNA ELISA Kits) expression and induces senescence hallmarks including telomere homeostasis in human primary fibroblasts.
results suggest that AKT1 (show AKT1 ELISA Kits), FTO (show FTO ELISA Kits), and AKTIP polymorphisms were not associated with obesity/overweight in Brazilians children.
FTS is involved in EGFR (show EGFR ELISA Kits)-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 (show ITK ELISA Kits) and cell migration by EGF (show EGF ELISA Kits) treatment. These results demonstrate a novel function for FTS in EGF (show EGF ELISA Kits)-mediated EMT (show ITK ELISA Kits) 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 (show AKT1 ELISA Kits) single markers and haplotypes, but not AKTIP polymorphisms or interactions between AKT1 (show AKT1 ELISA Kits) and AKTIP, are associated with increased risk for suicidal behavior in bipolar patients.
Ft1 protein is required for telomere maintenance.
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