anti-Chromosome 9 Open Reading Frame 72 (C9ORF72) Anticorps

Expansion of a hexanucleotide repeat in non-coding sequence between alternate 5' exons in transcripts from C9ORF72 is associated with 9p-linked ALS (amyotrophic lateral sclerosis) and FTD (frontotemporal dementia) (PMID: 21944778, 21944779). De plus, nous expédions C9ORF72 Protéines (5) et et beaucoup plus de produits pour cette protéine.

afficher tous les anticorps Gène GeneID UniProt
C9ORF72 203228 Q96LT7
C9ORF72 73205  
C9ORF72 313155 Q66HC3
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Top anti-C9ORF72 Anticorps sur anticorps-enligne.fr

Showing 10 out of 55 products:

Catalogue No. Reactivité Hôte Conjugué Application Images Quantité Livraison Prix Détails
Humain Lapin Inconjugué EIA, WB C9orf46 Antibody (C-term) western blot analysis in 293 cell line lysates (35µg/lane).This demonstrates the C9orf46 antibody detected the C9orf46 protein (arrow). 0.4 mL 6 to 8 Days
$484.00
Détails
Humain Lapin Inconjugué IHC, WB ABIN6272956 at 1/100 staining Mouse lung tissue by IHC-P. The sample was formaldehyde fixed and a heat mediated antigen retrieval step in citrate buffer was performed. The sample was then blocked and incubated with the antibody for 1.5 hours at 22°C. An HRP conjugated goat anti-rabbit antibody was used as the secondary. Western blot analysis of extracts of rat brain tissue, using C9orf72 antibody. 100 μL 11 to 12 Days
$390.77
Détails
Humain Lapin Inconjugué IF (p), IHC (p) Antigen: 2 µg/100 µL  Primary: Antiserum, 1:500, 1:1000, 1:2000, 1:4000, 1:8000, 1:16000, 1:32000;  Secondary: HRP conjugated Rabbit Anti-Goat IgG at 1: 5000;  TMB staining Read the data in Microplate Reader by 450nm. Formalin-fixed and paraffin embedded rat brain with labeled Anti-C9orf72 Polyclonal Antibody, Unconjugated (ABIN1386141) at 1:200, followed by conjugation to the secondary antibody and DAB staining 100 μL 3 to 7 Days
$317.90
Détails
Humain Lapin Inconjugué WB Western blot analysis of extracts of WiDr cells, using C9orf72 antibody. 100 μL 11 to 13 Days
$366.77
Détails
Humain Lapin Cy3 IF (p)   100 μL 14 to 21 Days
$416.90
Détails
Humain Lapin Cy5 IF (p)   100 μL 14 to 21 Days
$416.90
Détails
Humain Lapin Cy5.5 IF (p)   100 μL 14 to 21 Days
$416.90
Détails
Humain Lapin HRP IHC (p)   100 μL 14 to 21 Days
$416.90
Détails
Humain Lapin Cy7 IF (p)   100 μL 14 to 21 Days
$416.90
Détails
Humain Lapin Alexa Fluor 488 IF (p)   100 μL 14 to 21 Days
$416.90
Détails

anti-C9ORF72 Anticorps mieux référencés

  1. Human Polyclonal C9ORF72 Primary Antibody pour ICC, IF - ABIN4286688 : Snowden, Rollinson, Thompson, Harris, Stopford, Richardson, Jones, Gerhard, Davidson, Robinson, Gibbons, Hu, DuPlessis, Neary, Mann, Pickering-Brown: Distinct clinical and pathological characteristics of frontotemporal dementia associated with C9ORF72 mutations. dans Brain : a journal of neurology 2012 (PubMed)
    Show all 5 Pubmed References

Plus d’anticorps contre C9ORF72 partenaires d’interaction

Human Chromosome 9 Open Reading Frame 72 (C9ORF72) interaction partners

  1. the results from this study suggest that a psychiatric phenotype exists within C9orf72 kindreds

  2. Here the authors analyzed whether different cellular stressors promote repeat-associated non-AUG (RAN) translation of dipeptide repeats (DPRs) associated with the G4C2 hexanucleotide expansions in C9orf72, the most common genetic cause of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). They found that DPR translation was associated with neuronal excitation.

  3. The C9orf72 mutation of Frontotemporal Dementia association with psychotic symptoms and mainly associated with changes in the frontal cortex.

  4. This study showed that the c9orf72 mutation in Frontotemporal Dementia had the most atrophy of the CA4, CA1, and dentate gyrus regions showing the largest difference from controls.

  5. These data highlight that human PAF1C is an important transcriptional regulator of expanded G4C2 within C9orf72

  6. poly(GR)-induced mitochondrial defects are a major driver of disease initiation in C9ORF72-related ALS/FTD

  7. Our findings suggest that CpG-single nucleotide polymorphisms at the C6orf10/LOC101929163 locus might modify age of onset in C9orf72 carriers belonging to the entire amyotrophic lateral sclerosis-frontotemporal dementia spectrum by controlling DNA methylation and gene expression

  8. patients with a history of melanoma may have an increased probability of carrying a C9ORF72 repeat expansion

  9. Levels of mRNAs encoding EDN1 and its receptors, known to be elevated in ALS, were sharply increased by C9ORF72 KD.

  10. the combined expression of distinct C9orf72-derived dipeptide repeat species produces cellular outcomes and structural differences that are unique compared to the expression of a single DPR species, suggesting the complex biological interactions that occur when multiple DPR variants are simultaneously expressed.

  11. Study compared cerebral glucose metabolism of C9-familial frontotemporal lobar degeneration patients with matched non-carriers and with healthy controls (HCs). Voxel-based comparisons revealed a significant hypometabolic pattern in mutation carriers relative to HCs across widespread frontal and temporal areas, cingulate cortex, Rolandic operculum, caudate nuclei, and thalami.

  12. In the present study identified patients of SCA1, 2, 3, and 6 who also carried pathogenic C9orf72 repeat expansions.

  13. This study demonstrated that in presynaptic localization of C9orf72 protein and reduced protein levels in C9orf72 mutation carriers.

  14. The expression levels of HSF1 and protein chaperones are increased in C9ORF72-ALS/FTLD patients and in gain-of-function model systems.

  15. Study is the first report of a pair of amyotrophic lateral sclerosis -concordant dizygotic twins carrying a C9orf72 G4C2 expansion probably of intermediate length, and with a detailed clinical and genetic characterization.

  16. Restoring C9ORF72 levels or augmenting its function with constitutively active RAB5 or chemical modulators of RAB5 effectors rescued patient neuron survival and ameliorated neurodegenerative processes in both gain- and loss-of-function C9ORF72 mouse models.

  17. We used the CRISPR-Cas9 system to perform genome-wide gene-knockout screens for suppressors and enhancers of C9ORF72 dipeptide-repeat (DPR) protein toxicity in cells. One modifier, TMX2, modulated the ER-stress signature elicited by C9ORF72 DPRs in neurons and improved survival of induced motor neurons from patients with C9ORF72 ALS.

  18. The report confirms the notion that C9orf72 repeat expansions underlie a broad spectrum of neurodegenerative phenotypes. Relatively isolated agraphia in two cases with C9orf72 repeat expansions is a strong motivation to provide detailed and sophisticated oral and written language assessments that can be used to more precisely characterize early cognitive deficits in these heterogeneous conditions.

  19. Downregulation of C9orf72 in non-neuronal human cells overexpressing amyloid-beta protein precursor (AbetaPP) resulted in increased levels of secreted AbetaPP fragments and Abeta, while levels of AbetaPP or its C-terminal fragments (CTFs) remained unchanged. In neuronal cells, AbetaPP and C83 CTF levels were decreased upon C9orf72 knockdown, but those of secreted AbetaPP fragments or Abeta remained unchanged.

  20. Four of the ALS patients in this study possessed an expansion of the C9ORF72 gene, which has been linked to the presence of electrophysiological brain abnormalities, including cortical hyperexcitability, background rhythm slowing, and epileptic activity

Mouse (Murine) Chromosome 9 Open Reading Frame 72 (C9ORF72) interaction partners

  1. poly(GR)-induced mitochondrial defects are a major driver of disease initiation in C9ORF72-related ALS/FTD

  2. C9orf72 promoter activity is enriched in corticospinal and spinal motor neurons as well as in oligodendrocytes in brain regions that are affected in amyotrophic lateral sclerosis . These results suggest that cell autonomous changes in both neurons and glia may contribute to C9orf72-mediated disease

  3. Restoring C9ORF72 levels or augmenting its function with constitutively active RAB5 or chemical modulators of RAB5 effectors rescued patient neuron survival and ameliorated neurodegenerative processes in both gain- and loss-of-function C9ORF72 mouse models.

  4. A complex of C9ORF72 and p62 uses arginine methylation to eliminate stress granules by autophagy.

  5. C9orf72 acts by promoting the lysosomal degradation of coactivator-associated arginine methyltransferase 1 (CARM1), which in turn regulates autophagy-lysosomal functions and lipid metabolism.

  6. The findings suggest that C9orf72 functions as a potent negative regulator of autophagy, with a central role in coupling the cellular metabolic state with autophagy regulation.

  7. that epigenetic repression of the C9ORF72 HRE and nearby gene promoter could impede or delay motor neuron degeneration in C9-BAC mouse models of Amyotrophic Lateral Sclerosis

  8. Study generated C9orf72 deficient mice and showed that loss of C9orf72 leads to macrophage infiltration in multiple organs. Additionally, C9orf72 deficiency leads to autophagy defects and increased levels of many lysosomal proteins, supporting a critical role of C9orf72 in regulating autophagy/lysosomal pathway and inflammation in vivo.

  9. that C9ORF72 acts as a modulator of small GTPases in a pathway that regulates axonal actin dynamics

  10. target repeat-containing RNAs but preserve levels of mRNAs encoding C9ORF72 produced sustained reductions in RNA foci and dipeptide-repeat proteins

  11. report a BAC mouse model of C9orf72 ALS/FTD that shows decreased survival, paralysis, muscle denervation, motor neuron loss, anxiety-like behavior, and cortical and hippocampal neurodegeneration

  12. These results demonstrate that the C9orf72-SMCR8 protein complex functions in the regulation of metabolism and provide evidence that loss of C9orf72 function may contribute to the pathogenesis of relevant diseases

  13. two independent mouse lines lacking the C9orf72 ortholog (3110043O21Rik) in all tissues developed normally and aged without motor neuron disease. Instead, C9orf72 null mice developed progressive splenomegaly and lymphadenopathy with accumulation of engorged macrophage-like cells.

C9ORF72 profil antigène

Profil protéine

Expansion of a hexanucleotide repeat in non-coding sequence between alternate 5' exons in transcripts from this gene is associated with 9p-linked ALS (amyotrophic lateral sclerosis) and FTD (frontotemporal dementia) (PMID: 21944778, 21944779). Multiple transcript variants encoding different isoforms have been found for this gene.

Gene names and symbols associated with C9ORF72

  • chromosome Z C9orf72 homolog (CZH9orf72) anticorps
  • chromosome 9 open reading frame 72 (C9orf72) anticorps
  • RIKEN cDNA 3110043O21 gene (3110043O21Rik) anticorps
  • similar to RIKEN cDNA 3110043O21 (RGD1359108) anticorps
  • chromosome 9 open reading frame 72 L homeolog (c9orf72.L) anticorps
  • AI840585 anticorps
  • ALSFTD anticorps
  • c9orf72 anticorps
  • CZH9orf72 anticorps
  • FTDALS anticorps

Protein level used designations for C9ORF72

protein C9orf72 , protein C9orf72 homolog , uncharacterized protein LOC496290

GENE ID SPECIES
427370 Gallus gallus
203228 Homo sapiens
73205 Mus musculus
313155 Rattus norvegicus
496290 Xenopus laevis
Fournisseurs de qualité sélectionnés pour anti-C9ORF72 (C9ORF72) Anticorps
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