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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 Kits (33) and TAR DNA Binding Protein Proteins (14) and many more products for this protein.
Showing 10 out of 161 products:
Human Polyclonal TARDBP Primary Antibody for EIA, IF - ABIN500883
Buratti, Dörk, Zuccato, Pagani, Romano, Baralle: Nuclear factor TDP-43 and SR proteins promote in vitro and in vivo CFTR exon 9 skipping. in The EMBO journal 2001
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Human Polyclonal TARDBP Primary Antibody for IHC (fro), WB - ABIN784609
Forman, Trojanowski, Lee: TDP-43: a novel neurodegenerative proteinopathy. in Current opinion in neurobiology 2008
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Human Monoclonal TARDBP Primary Antibody for EIA, IHC (p) - ABIN317572
Kabashi, Valdmanis, Dion, Spiegelman, McConkey, Vande Velde, Bouchard, Lacomblez, Pochigaeva, Salachas, Pradat, Camu, Meininger, Dupre, Rouleau: TARDBP mutations in individuals with sporadic and familial amyotrophic lateral sclerosis. in Nature genetics 2008
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Chicken Polyclonal TARDBP Primary Antibody for IHC, WB - ABIN2780848
Buratti, Brindisi, Giombi, Tisminetzky, Ayala, Baralle: TDP-43 binds heterogeneous nuclear ribonucleoprotein A/B through its C-terminal tail: an important region for the inhibition of cystic fibrosis transmembrane conductance regulator exon 9 splicing. in The Journal of biological chemistry 2005
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Chicken Polyclonal TARDBP Primary Antibody for IHC, WB - ABIN2780849
Polymenidou, Lagier-Tourenne, Hutt, Huelga, Moran, Liang, Ling, Sun, Wancewicz, Mazur, Kordasiewicz, Sedaghat, Donohue, Shiue, Bennett, Yeo, Cleveland: Long pre-mRNA depletion and RNA missplicing contribute to neuronal vulnerability from loss of TDP-43. in Nature neuroscience 2011
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Human Polyclonal TARDBP Primary Antibody for IF, WB - ABIN318898
Ou, Wu, Harrich, García-Martínez, Gaynor: Cloning and characterization of a novel cellular protein, TDP-43, that binds to human immunodeficiency virus type 1 TAR DNA sequence motifs. in Journal of virology 1995
Human Polyclonal TARDBP Primary Antibody for IF, IHC (p) - ABIN657685
Kim, Shanware, Bowler, Tibbetts: Amyotrophic lateral sclerosis-associated proteins TDP-43 and FUS/TLS function in a common biochemical complex to co-regulate HDAC6 mRNA. in The Journal of biological chemistry 2010
Human Polyclonal TARDBP Primary Antibody for ELISA, WB - ABIN334503
Zhang, Xu, Dickey, Buratti, Baralle, Bailey, Pickering-Brown, Dickson, Petrucelli: Progranulin mediates caspase-dependent cleavage of TAR DNA binding protein-43. in The Journal of neuroscience : the official journal of the Society for Neuroscience 2007
TDP-43 does not critically regulate expression or splicing of tau in Alzheimer's disease suggesting that TDP-43 contributes to Alzheimer's disease through mechanisms independent of tau.
Study identifies a common mechanism of transport into neurites of proteins linked to the pathology of Alzheimer's disease (i.e. sAPP) and ALS (show IGFALS Antibodies) (i.e. FUS (show FUS Antibodies), TDP-43 and SOD1 (show SOD1 Antibodies))
RNA binding proteins TDP-43 and FUS (show FUS Antibodies) do not consistently fit the currently characterised inclusion models suggesting that cells have a larger repertoire for generating inclusions than currently thought.
TDP-43 does have dynamic inter-domain interactions, which are coordinated by the intrinsically-disordered prion (show PRNP Antibodies)-like domain.
Data indicate that the structure of TAR DNA-binding protein-43 (TDP-43)consists of an alpha-helix and six beta-strands.
Knockdown of TDP-43 results in an increase in viral titers, suggesting a protective role for TDP-43 in CVB3 infection.
Data suggest that TRIM16 (show TRIM16 Antibodies) and TDP43 are both good prognosis indicators; data shows that TRIM16 (show TRIM16 Antibodies) inhibits cancer cell viability by a novel mechanism involving interaction and stabilisation of TDP43 with consequent effects on E2F1 (show E2F1 Antibodies) and pRb (show RB1 Antibodies) proteins.
results support a model whereby dFMRP (show FMR1 Antibodies) 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
Data demonstrate the existence of a physiological decrease of TDP-43/TBPH levels with aging in brain tissue both in wild-type mice and flies, showing that it is an evolutionary conserved phenomenon
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 Antibodies) dysregulation in neurons can drive NF-kappaB (show NFKB1 Antibodies) activation and cytosolic TDP-43 aggregation.
These findings demonstrate a role for PABPN1 (show PABPN1 Antibodies) in rescuing several cytopathological features of TDP-43 proteinopathy by increasing the turnover of pathologic proteins.
identifies DDX58 (show DDX58 Antibodies) 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 Antibodies), Noggin (show NOG Antibodies), and Numb (show NUMB Antibodies) proteins. we found that Shh (show SHH Antibodies) and Noggin (show NOG Antibodies) could affect motor performance and that these proteins could be associated with both TDP-43 and Numb (show NUMB Antibodies)
The ability of TDP-43 to promote CD14 (show CD14 Antibodies)-mediated activation of microglial NF-kappaB (show NFKB1 Antibodies) and AP-1 (show JUN Antibodies) pathways, as well as the NLRP3 (show NLRP3 Antibodies) inflammasome.
Depletion of TDP-43 leads to a dramatic reduction in the RNA processing and the protein levels of IL-6 (show IL6 Antibodies) in serum.
our results reveal a previously unrecognized non-cell-autonomous mechanism in TDP-43-mediated neurodegeneration, identifying COX-2 (show COX2 Antibodies)-PGE2 as the molecular events of microglia- but not astrocyte-initiated neurotoxicity
Data indicate a method for site-directed single nucleotide editing in two disease-related genes, DNA binding protein (show CNBP Antibodies) tardbp and RNA binding protein fus (show FUS Antibodies).
Loss of ALS-associated TDP-43 in zebrafish causes muscle degeneration, vascular dysfunction, and reduced motor neuron axon outgrowth.
TARDBP and FUS (show FUS Antibodies) act in a pathogenic pathway that is independent of SOD1 (show SOD1 Antibodies).
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