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

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). Zusätzlich bieten wir Ihnen C9ORF72 Proteine (5) und und viele weitere Produktgruppen zu diesem Protein an.

Alle Antikörper anzeigen Gen GeneID UniProt
C9ORF72 203228 Q96LT7
C9ORF72 73205  
C9ORF72 313155 Q66HC3
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Top anti-C9ORF72 Antikörper auf

Showing 10 out of 55 products:

Katalog Nr. Reaktivität Wirt Konjugat Applikation Bilder Menge Lieferzeit Preis Details
Human Kaninchen Unkonjugiert 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 bis 8 Tage
Human Kaninchen Unkonjugiert 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 bis 12 Tage
Human Kaninchen Unkonjugiert 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 bis 7 Tage
Human Kaninchen Unkonjugiert WB Western blot analysis of extracts of WiDr cells, using C9orf72 antibody. 100 μL 11 bis 13 Tage
Human Kaninchen Cy3 IF (p)   100 μL 14 bis 21 Tage
Human Kaninchen Cy5 IF (p)   100 μL 14 bis 21 Tage
Human Kaninchen Cy5.5 IF (p)   100 μL 14 bis 21 Tage
Human Kaninchen HRP IHC (p)   100 μL 14 bis 21 Tage
Human Kaninchen Cy7 IF (p)   100 μL 14 bis 21 Tage
Human Kaninchen Alexa Fluor 488 IF (p)   100 μL 14 bis 21 Tage

Am meisten referenzierte anti-C9ORF72 Antikörper

  1. Human Polyclonal C9ORF72 Primary Antibody für 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. in Brain : a journal of neurology 2012 (PubMed)
    Show all 5 Pubmed References

Weitere Antikörper gegen C9ORF72 Interaktionspartner

Human Chromosome 9 Open Reading Frame 72 (C9ORF72) Interaktionspartner

  1. Results found that brains of patients with amyotrophic lateral sclerosis/frontotemporal dementia (ALS/FTD) and carrying the C9 repeat expansion in C9orf72 gene show derepression of epigenetically silenced genes and insolubility of PRC2.

  2. presenting a potential therapeutic target for C9orf72-related amyotrophic lateral sclerosis

  3. The data of this study confirmed the association between deletions within GC-rich region and the GGGGCC expansion in Italian and Turkish cases.

  4. Repeat expansion in theC9orf72gene is the mostcommon cause of the neurodegenerative disorderamyotrophic lateral sclerosis (C9-ALS) and is linkedto the unconventional translation of five dipeptide-repeat polypeptides (DPRs).

  5. C9orf72 repeat expansion carriers had the lowest prevalence of immunological diseases in comparison with control groups.

  6. that C9orf72 repeat expansion does not coexist with HTT repeat expansion and that C9orf72 repeat expansion testing is unnecessary for patients with HD

  7. Study found mutations in either SOD1 or C9orf72 in 9.2% of patients and accounted for 40% of familial amyotrophic lateral sclerosis and 5.2% of sporadic amyotrophic lateral sclerosis in a Portuguese population. SOD1 mutations were rare (0.83%), but a novel and probably disease-causing mutation was identified.

  8. This results of this study contribute to a better understanding of the preclinical phase of C9orf72 disease and of the respective contribution of magnetic resonance biomarkers.

  9. A genetic study confirmed a C9ORF72 hexanucleotide expansion in patient with frontotemporal dementia.

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

  11. 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.

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

  13. 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.

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

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

  16. 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

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

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

  19. 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.

  20. 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.

Mouse (Murine) Chromosome 9 Open Reading Frame 72 (C9ORF72) Interaktionspartner

  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 Antigen-Profil

Protein Überblick

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.

Genbezeichner und Symbole assoziert mit C9ORF72

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

Bezeichner auf Proteinebene für C9ORF72

protein C9orf72 , protein C9orf72 homolog , uncharacterized protein LOC496290

427370 Gallus gallus
203228 Homo sapiens
73205 Mus musculus
313155 Rattus norvegicus
496290 Xenopus laevis
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