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FUS encodes a multifunctional protein component of the heterogeneous nuclear ribonucleoprotein (hnRNP) complex. Zusätzlich bieten wir Ihnen FUS Antikörper (45) und FUS Proteine (2) und viele weitere Produktgruppen zu diesem Protein an.
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A molecular docking and dynamics study concluded that R521C and R521H mutations in FUS result in weak binding with Karyopherin-beta2 leading to amyotrophic lateral sclerosis.
both FUS and TDP43 (zeige TARDBP ELISA Kits) colocalize with active RNA polymerase II at sites of DNA damage along with the DNA damage repair protein, BRCA1, and FUS and TDP43 (zeige TARDBP ELISA Kits) participate in the prevention or repair of R loop-associated DNA damage, a manifestation of aberrant transcription and/or RNA processing
FUS mutations were significantly more common among mainland Chinese patients than those among Caucasian populations (p=6.8x10-3). The high frequency of FUS mutations in FALS and SALS in mainland China is another genetic feature distinct from Caucasians.
The impairment of PARP (zeige COL11A2 ELISA Kits)-dependent DNA damage response (DDR (zeige DDR1 ELISA Kits)) signaling due to mutations in the FUS nuclear localization sequence induces additional cytoplasmic FUS mislocalization which in turn results in neurodegeneration and FUS aggregate formation in amyotrophic lateral sclerosis.
ALS (zeige IGFALS ELISA Kits)-associated mutations enhance FUS protein propagation in Drosophila neurons.
juvenile ALS (zeige IGFALS ELISA Kits) linked to FUS mutations represent a specific entity different from both classical juvenile ALS (zeige IGFALS ELISA Kits) and adult ALS (zeige IGFALS ELISA Kits) linked to FUS gene
Motor neurons expressing FUS with the P525L or the R521H mutation showed cytoplasmic mislocalization of FUS, hypoexcitability, and axonal transport defects.
Results suggest that RBM45 (zeige RBM45 ELISA Kits) serves as a negative regulator to prevent FUS-mediated excessive recruitment of HDAC1 (zeige HDAC1 ELISA Kits) to the sites of DNA damage.
Authors found that FUS, EWS (zeige EWSR1 ELISA Kits) and TAF15 expression is differentially regulated during brain development, both in time and in space. In particular, this study identifies a fine-tuned regulation of FUS and EWS (zeige EWSR1 ELISA Kits) during neuronal differentiation.
The review describes the main physiological functions of FUS and considers evidence for each of the theories of amyotrophic lateral sclerosis pathogenesis.
These two proteins were up-regulated in both HD and FUS/TLS heterozygote mice.
Study established that Fus1 (zeige TUSC2 ELISA Kits) KO mice suffer from the age-related hearing loss (ARHL) of strial origin, making this model a valuable tool for studying mitochondrial/oxidative mechanisms of age-related hearing decline. The model describes the phenotype of premature hearing loss of strial etiology based on Fus1 (zeige TUSC2 ELISA Kits) loss-mediated mitochondrial dysfunction, and identify the target cells and tissues in the inner ear.
Study characterizes a heterozygous knock-in mouse model of ALS and demonstrates that mutations in FUS result in a toxic gain of function leading to motor neuron disease through cell autonomous and non-cell autonomous mechanisms; shows that mutant FUS triggers toxic events in both motor neurons and neighboring cells to elicit motor neuron disease.
FUS-induced reductions to ER-mitochondria associations and are linked to activation of glycogen synthase kinase-3beta (GSK-3beta), a kinase already strongly associated with ALS/FTD (zeige FTL ELISA Kits).
our findings indicate that cytoplasmic FUS mislocalization not only leads to nuclear loss of function, but also triggers motor neuron death through a toxic gain of function within motor neurons.
The data of this study support the notion that expression of cytoplasmically mislocalized FUS with compromised RNA-binding capacity causes particularly prominent and harmful FUS pathology in the mouse nervous system.
These results highlight the pivotal role of FUS in regulating GluA1 (zeige GRIA1 ELISA Kits) mRNA stability, post-synaptic function and fronto-temporal lobar degeneration-like animal behaviors.
these studies establish potentially converging disease mechanisms in amyotrophic lateral sclerosis (ALS) and spinal muscular atrophy, with ALS-causative mutants acquiring properties representing both gain and loss of function.
FUS/TLS depletion causes phenotypes possibly related to neuropsychiatric and neurodegenerative conditions, but distinct from ALS and ET, together with specific alterations in RNA metabolisms.
This gene encodes a multifunctional protein component of the heterogeneous nuclear ribonucleoprotein (hnRNP) complex. The hnRNP complex is involved in pre-mRNA splicing and the export of fully processed mRNA to the cytoplasm. This protein belongs to the FET family of RNA-binding proteins which have been implicated in cellular processes that include regulation of gene expression, maintenance of genomic integrity and mRNA/microRNA processing. Alternative splicing results in multiple transcript variants. Defects in this gene result in amyotrophic lateral sclerosis type 6.
75 kDa DNA-pairing protein
, RNA-binding protein FUS
, fus-like protein
, fusion gene in myxoid liposarcoma
, heterogeneous nuclear ribonucleoprotein P2
, oncogene FUS
, oncogene TLS
, translocated in liposarcoma protein
, fusion, derived from t(12;16) malignant liposarcoma
, hnRNP P2
, pigpen protein
, protein pigpen
, translocated in liposarcoma
, fusion (involved in t(12;16) in malignant liposarcoma)
, 16) in malignant liposarcoma)
, 16) malignant liposarcoma
, fusion (involved in t(12
, fusion, derived from t(12