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HIV-1, the causative agent of acquired immunodeficiency syndrome (AIDS), contains an RNA genome that produces a chromosomally integrated DNA during the replicative cycle. Additionally we are shipping TAR DNA Binding Protein Antibodies (160) and TAR DNA Binding Protein Proteins (14) and many more products for this protein.
Showing 10 out of 33 products:
results support a model whereby dFMRP (show FMR1 ELISA Kits) can modulate the neurotoxicity caused by TDP-43 overexpression
TDP-43 pathology in the basal forebrain is strongly associated with hippocampal sclerosis-aging.
Results suggest that functional deficits in iTDP-43(A315T) mice are at least in part a direct and transient effect of the presence of TDP-43(A315T) and illustrate the compensatory capacity of compromised neurons once transgenic TDP-43 is removed
Even after neurodegeneration and onset of motor dysfunction, removal of cytoplasmic pathological TDP-43 and the concomitant return of nuclear TDP-43 led to neuron preservation, muscle re-innervation and functional recovery
Results demonstrate that ALS-mutant forms of TDP-43, FUS, and SOD1 all perturb protein transport in the early secretory pathway between ER and Golgi compartments, and imply that restoring Rab1-mediated ER-Golgi transport is a novel ALS therapeutic target
ALS (show IGFALS ELISA Kits)-FTD (show FTL ELISA Kits)-CSF (show CSF2 ELISA Kits) exposure generates TDP-43 aggregates in glioblastoma cells through exosomes and tunneling nanotube -like structures
Expression of truncated hyperactive form of CKIdelta (show CSNK1D ELISA Kits) causes mislocalization and aggregation of TDP-43 in cultured cells.
This study identified variants in TARDBP across a range of phenotypes (Alzheimer's Disease , Alzheimer's Disease and cerebrovascular disease,frontotemporal dementia and progressive supranuclear palsy.
The TARDBP Ala382Thr mutation does not play a major role in multiple sclerosis pathogenesis in the Sardinian population.
TDP-43 may play an important role in regulating the levels of NF-kappaB (show NFKB1 ELISA Kits) activity by controlling the nuclear translocation of p65 (show GORASP1 ELISA Kits).
This study demonistrated that proprioceptive nerve endings in muscles revealed early and alterations at Ia/II proprioceptive nerve endings in muscle spindles and in the absence of alterations in alpha-motor axons in TDP43(A315T) transgenic mice.
UBQLN2 (show UBQLN2 ELISA Kits) dysregulation in neurons can drive NF-kappaB (show NFKB1 ELISA Kits) activation and cytosolic TDP-43 aggregation.
These findings demonstrate a role for PABPN1 (show PABPN1 ELISA Kits) in rescuing several cytopathological features of TDP-43 proteinopathy by increasing the turnover of pathologic proteins.
identifies DDX58 (show DDX58 ELISA Kits) and MTHFSD as two TDP-43 targets that are misregulated in amyotrophic lateral sclerosis. 1
Valproate Attenuates 25-kDa C-Terminal Fragment of TDP-43-Induced Neuronal Toxicity via Suppressing Endoplasmic Reticulum Stress and Activating Autophagy.
we observed a glial reaction and an activity-dependent modification of Shh (show SHH ELISA Kits), Noggin (show NOG ELISA Kits), and Numb (show NUMB ELISA Kits) proteins. we found that Shh (show SHH ELISA Kits) and Noggin (show NOG ELISA Kits) could affect motor performance and that these proteins could be associated with both TDP-43 and Numb (show NUMB ELISA Kits)
The ability of TDP-43 to promote CD14 (show CD14 ELISA Kits)-mediated activation of microglial NF-kappaB (show NFKB1 ELISA Kits) and AP-1 (show JUN ELISA Kits) pathways, as well as the NLRP3 (show NLRP3 ELISA Kits) inflammasome.
Depletion of TDP-43 leads to a dramatic reduction in the RNA processing and the protein levels of IL-6 (show IL6 ELISA Kits) in serum.
our results reveal a previously unrecognized non-cell-autonomous mechanism in TDP-43-mediated neurodegeneration, identifying COX-2 (show COX2 ELISA Kits)-PGE2 as the molecular events of microglia- but not astrocyte-initiated neurotoxicity
Results reveal a previously underappreciated complexity to TDP-43 regulated splicing and suggest that loss of TDP-43 autoregulatory capacity may contribute to the pathogenesis of amyotrophic lateral sclerosis.
Data indicate a method for site-directed single nucleotide editing in two disease-related genes, DNA binding protein (show CNBP ELISA Kits) tardbp and RNA binding protein fus (show FUS ELISA Kits).
Loss of ALS-associated TDP-43 in zebrafish causes muscle degeneration, vascular dysfunction, and reduced motor neuron axon outgrowth.
TARDBP and FUS (show FUS ELISA Kits) act in a pathogenic pathway that is independent of SOD1 (show SOD1 ELISA Kits).
HIV-1, the causative agent of acquired immunodeficiency syndrome (AIDS), contains an RNA genome that produces a chromosomally integrated DNA during the replicative cycle. Activation of HIV-1 gene expression by the transactivator Tat is dependent on an RNA regulatory element (TAR) located downstream of the transcription initiation site. The protein encoded by this gene is a transcriptional repressor that binds to chromosomally integrated TAR DNA and represses HIV-1 transcription. In addition, this protein regulates alternate splicing of the CFTR gene. A similar pseudogene is present on chromosome 20.
TAR DNA binding protein
, TAR DNA-binding protein 43
, Tardbp protein
, TAR DNA-binding protein-43