Anti-LYRIC antibody (ab76742)
- Product nameAnti-LYRIC antibodySee all LYRIC primary antibodies ...
- DescriptionRabbit polyclonal to LYRIC
- Tested applicationsICC/IF, IHC-P, IHC-Fr, WB more details
- Species reactivityReacts with: Human
Predicted to work with: Mouse, Rat
Synthetic peptide derived from the N terminal domain of human LYRIC protein
- Storage instructionsShipped at 4°C. Upon delivery aliquot and store at -20°C. Avoid repeated freeze / thaw cycles.
- Storage bufferPreservative: None
Constituents: Whole serum
- PurityWhole antiserum
- Clonality Polyclonal
- Research Areas
Our Abpromise guarantee covers the use of ab76742 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
|ICC/IF||ICC/IF: Use a concentration of 5 µg/ml.|
|IHC-P||IHC-P: 1/50 - 1/200.|
|IHC-Fr||IHC-Fr: 1/50 - 1/200.|
|WB||WB: 1/100 - 1/1000. Detects a band of approximately 65 kDa (predicted molecular weight: 65 kDa).|
- FunctionDownregulates SLC1A2/EAAT2 promoter activity when expressed ectopically. Activates the nuclear factor kappa-B (NF-kappa-B) transcription factor. Promotes anchorage-independent growth of immortalized melanocytes and astrocytes which is a key component in tumor cell expansion. Promotes lung metastasis and also has an effect on bone and brain metastasis, possibly by enhancing the seeding of tumor cells to the target organ endothelium. Induces chemoresistance.
- Tissue specificityWidely expressed with highest levels in muscle-dominating organs such as skeletal muscle, heart, tongue and small intestine and in endocrine glands such as thyroid and adrenal gland. Overexpressed in various cancers including breast, brain, prostate, melanoma and glioblastoma multiforme.
- Cellular localizationEndoplasmic reticulum membrane. Nucleus membrane. Cell junction > tight junction. Nucleus > nucleolus. Cytoplasm > perinuclear region. In epithelial cells, recruited to tight junctions (TJ) during the maturation of the TJ complexes. A nucleolar staining may be due to nuclear targeting of an isoform lacking the transmembrane domain (By similarity). TNF-alpha causes translocation from the cytoplasm to the nucleus.
- 3D3 antibody
- 3D3/lyric antibody
- AEG 1 antibody
- AEG-1 antibody
- AEG1 antibody
- Astrocyte elevated gene 1 antibody
- Astrocyte elevated gene-1 protein antibody
- LYRIC antibody
- LYRIC/3D3 antibody
- LYRIC_HUMAN antibody
- Lysine rich CEACAM1 associated protein antibody
- Lysine rich CEACAM1 co isolated protein antibody
- Lysine-rich CEACAM1 co-isolated protein antibody
- metadherin antibody
- metastasis adhesion protein antibody
- MTDH antibody
- Protein LYRIC antibody
Anti-LYRIC antibody images
All lanes : Anti-LYRIC antibody (ab76742) at 1/500 dilution
Lane 1 :
Heart (Human) Tissue Lysate - adult normal tissue (ab29431)
Lane 2 : MCF7 (Human breast adenocarcinoma cell line) Whole Cell Lysate
Lysates/proteins at 10 µg/ml per lane.
Goat polyclonal Secondary Antibody to Rabbit IgG - H&L (HRP), pre-adsorbed (ab97080) at 1/5000 dilution
developed using the ECL technique
Performed under reducing conditions.
Predicted band size : 65 kDa
Observed band size : 65 kDa
Additional bands at : 32 kDa,63 kDa,67 kDa (possible post-translational modification). We are unsure as to the identity of these extra bands.
Exposure time : 3 minutes
ICC/IF image of ab76742 stained Mcf7 cells. The cells were 4% formaldehyde fixed (10 min) and then incubated in 1%BSA / 10% normal goat serum / 0.3M glycine in 0.1% PBS-Tween for 1h to permeabilise the cells and block non-specific protein-protein interactions. The cells were then incubated with the antibody (ab76742, 5µg/ml) overnight at +4°C. The secondary antibody (green) was Alexa Fluor® 488 goat anti-rabbit IgG (H+L) used at a 1/1000 dilution for 1h. Alexa Fluor® 594 WGA was used to label plasma membranes (red) at a 1/200 dilution for 1h. DAPI was used to stain the cell nuclei (blue) at a concentration of 1.43µM.
References for Anti-LYRIC antibody (ab76742)
ab76742 has not yet been referenced specifically in any publications.