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SCYL1 deficiency can cause recurrent low-GGT cholestatic liver dysfunction in conjunction with a variable neurological phenotype
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findings indicate that SCYL1 does not contribute to REST turnover and thus do not support a previous study suggesting a role for SCYL1 in mediating REST degradation
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Disruptive SCYL1 mutations underlie a syndrome characterized by recurrent episodes of liver failure, peripheral neuropathy, cerebellar atrophy, and ataxia.
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Data identified the large GTPase dynamin2 as an interacting protein of NTKL, which might be responsible for the phenotype alterations caused by NTKL overexpression, such as cytokinesis failure, increased cell motility and abnormal of cell division.
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Data reveal that Scyl1 is a key organizer of a subset of the COPI machinery.
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TEIF is a downstream effector in EGF/PI3K/Akt signaling.
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TEIF as a novel MSP58-interacting protein.
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suggested that the interaction of SCYL1BP1/Pirh2 could accelerate Pirh2 degradation through an ubiquitin-dependent pathway. SCYL1BP1 may function as an important tumor suppressor gene in HCC development
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TEIF protein and centrosome amplification is commonly found in colorectal tumors. The expression level of TEIF is related to tumor histological grade and malignant degree.
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Scyl1 interacts with 58K/formiminotransferase cyclodeaminase (FTCD) and golgin p115, and is required for the maintenance of Golgi morphology
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Scyl1 participates in the nuclear aminoacylation-dependent tRNA export pathway.
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SCYL1-BP1 can be ubiquitinated and degraded by Pirh2 but not by MDM2, which suggests that SCYL1-BP1 can be regulated by Pirh2.
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NTKL is involved in centrosome-related cellular functions
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Molecular cloning of telomerase transcriptional elements-interacting factor,(TEIF). TEIF may take part in the transcriptional activation of hTERT.
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TEIF could specifically activate transcription of beta-pol promoter, but not that of DNA polymerase alpha or delta promoter. The responsible sequences for binding of TEIF were revealed
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TEIF functions as a centrosome regulator. Its participation in DNA damage response, including telomere dysfunction and tumorigenesis.
