Nogo Receptor Antibody - #DF13593

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Product: Nogo Receptor Antibody
Catalog: DF13593
Description: Rabbit polyclonal antibody to Nogo Receptor
Application: WB IHC
Reactivity: Human, Mouse, Rat
Prediction: Pig, Horse
Mol.Wt.: 50kDa; 51kD(Calculated).
Uniprot: Q9BZR6
RRID: AB_2846612

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Related Downloads
MS Report
HPLC Report
MSDS
Data Sheet
COA
Protocols
WB Handbook
IHC Protocol
IF/ICC Protocol

Product Info

Source:
Rabbit
Application:
WB 1:500-1:2000, IHC 1:50-1:200
*The optimal dilutions should be determined by the end user.
*Tips:

WB: For western blot detection of denatured protein samples. IHC: For immunohistochemical detection of paraffin sections (IHC-p) or frozen sections (IHC-f) of tissue samples. IF/ICC: For immunofluorescence detection of cell samples. ELISA(peptide): For ELISA detection of antigenic peptide.

Reactivity:
Human,Mouse,Rat
Prediction:
Pig(88%), Horse(88%)
Clonality:
Polyclonal
Specificity:
Nogo Receptor Antibody detects endogenous levels of total Nogo Receptor.
RRID:
AB_2846612
Cite Format: Affinity Biosciences Cat# DF13593, RRID:AB_2846612.
Conjugate:
Unconjugated.
Purification:
The antiserum was purified by peptide affinity chromatography using SulfoLink™ Coupling Resin (Thermo Fisher Scientific).
Storage:
Rabbit IgG in phosphate buffered saline , pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol. Store at -20 °C. Stable for 12 months from date of receipt.
Alias:

Fold/Unfold

NgR; Nogo 66 receptor; Nogo receptor; Nogor; Reticulon 4 receptor; Rtn4r; UNQ330/PRO526;

Immunogens

Immunogen:
Uniprot:

Q9BZR6(RTN4R_HUMAN) >>Visit HPA database.

Gene(ID):
RTN4R(65078)
Expression:
Q9BZR6 RTN4R_HUMAN:

Widespread in the brain but highest levels in the gray matter. Low levels in heart and kidney; not expressed in oligodendrocytes (white matter).

Sequence:
MKRASAGGSRLLAWVLWLQAWQVAAPCPGACVCYNEPKVTTSCPQQGLQAVPVGIPAASQRIFLHGNRISHVPAASFRACRNLTILWLHSNVLARIDAAAFTGLALLEQLDLSDNAQLRSVDPATFHGLGRLHTLHLDRCGLQELGPGLFRGLAALQYLYLQDNALQALPDDTFRDLGNLTHLFLHGNRISSVPERAFRGLHSLDRLLLHQNRVAHVHPHAFRDLGRLMTLYLFANNLSALPTEALAPLRALQYLRLNDNPWVCDCRARPLWAWLQKFRGSSSEVPCSLPQRLAGRDLKRLAANDLQGCAVATGPYHPIWTGRATDEEPLGLPKCCQPDAADKASVLEPGRPASAGNALKGRVPPGDSPPGNGSGPRHINDSPFGTLPGSAEPPLTAVRPEGSEPPGFPTSGPRRRPGCSRKNRTRSHCRLGQAGSGGGGTGDSEGSGALPSLTCSLTPLGLALVLWTVLGPC

Predictions

Predictions:

Score>80(red) has high confidence and is suggested to be used for WB detection. *The prediction model is mainly based on the alignment of immunogen sequences, the results are for reference only, not as the basis of quality assurance.

Species
Results
Score
Pig
88
Horse
88
Bovine
75
Sheep
75
Dog
0
Xenopus
0
Zebrafish
0
Chicken
0
Rabbit
0
Model Confidence:
High(score>80) Medium(80>score>50) Low(score<50) No confidence

PTMs - Q9BZR6 As Substrate

Site PTM Type Enzyme
N82 N-Glycosylation
N179 N-Glycosylation

Research Backgrounds

Function:

Receptor for RTN4, OMG and MAG. Functions as receptor for the sialylated gangliosides GT1b and GM1. Besides, functions as receptor for chondroitin sulfate proteoglycans (By similarity). Can also bind heparin (By similarity). Intracellular signaling cascades are triggered via the coreceptor NGFR. Signaling mediates activation of Rho and downstream reorganization of the actin cytoskeleton. Mediates axonal growth inhibition. Plays a role in regulating axon regeneration and neuronal plasticity in the adult central nervous system. Plays a role in postnatal brain development. Required for normal axon migration across the brain midline and normal formation of the corpus callosum. Protects motoneurons against apoptosis; protection against apoptosis is probably mediated via interaction with MAG. Acts in conjunction with RTN4 and LINGO1 in regulating neuronal precursor cell motility during cortical development. Like other family members, plays a role in restricting the number dendritic spines and the number of synapses that are formed during brain development.

PTMs:

N-glycosylated. O-glycosylated. Contains terminal sialic acid groups on its glycan chains.

Subcellular Location:

Cell membrane>Lipid-anchor. Membrane raft. Cell projection>Dendrite. Cell projection>Axon. Perikaryon.
Note: Detected along dendrites and axons, close to synapses, but clearly excluded from synapses.

Extracellular region or secreted Cytosol Plasma membrane Cytoskeleton Lysosome Endosome Peroxisome ER Golgi apparatus Nucleus Mitochondrion Manual annotation Automatic computational assertionSubcellular location
Tissue Specificity:

Widespread in the brain but highest levels in the gray matter. Low levels in heart and kidney; not expressed in oligodendrocytes (white matter).

Subunit Structure:

Homodimer. Interacts with MAG. Interacts with RTN4. Interacts with NGFR. Interacts with LINGO1. Interacts with KIAA0319L. Interacts with OLFM1; this inhibits interaction with LINGO1 and NGFR (By similarity). Interacts with OMG.

Family&Domains:

Belongs to the Nogo receptor family.

References

1). Focal ischemic stroke modifies microglia-derived exosomal miRNAs: potential role of mir-212-5p in neuronal protection and functional recovery. Biological Research, 2023 (PubMed: 37789455) [IF=6.7]

Application: WB    Species: Rat    Sample:

Fig. 6 MiR-212-5p promotes synaptic plasticity and attenuates axon degeneration at 7 days following MCAO/R. A Ultrastructures of the synapses in the ischemic penumbra analysed using TEM. Scale bar = 2 μm. B Schematic of the presynaptic (violet) and postsynaptic (green) structures. C The number of synapses in the ischemic penumbra of the cortex in each group. D Width of the synaptic space (nm). n = 3 per group. E Immunofluorescence staining shows MAP-2 (in green) expression in the ischemic penumbra of the cortex. Nuclei were stained with DAPI and are visualised in blue. Scale bar = 50 μm. F Representative images of western blots for Nogo-A, NgR, and GAP-43. G Quantitative analysis of the western blot results. n = 4–6 per group. H-J Immunofluorescence staining was performed to show the presence of Nogo-A, NgR and β III tubulin in the ischemic penumbra of the cortex. Nuclei were stained with DAPI and are visualised in blue. Scale bar =, 50 μm. The data are presented as the means ± SEM. *P 

Application: IF/ICC    Species: Rat    Sample:

Fig. 6 MiR-212-5p promotes synaptic plasticity and attenuates axon degeneration at 7 days following MCAO/R. A Ultrastructures of the synapses in the ischemic penumbra analysed using TEM. Scale bar = 2 μm. B Schematic of the presynaptic (violet) and postsynaptic (green) structures. C The number of synapses in the ischemic penumbra of the cortex in each group. D Width of the synaptic space (nm). n = 3 per group. E Immunofluorescence staining shows MAP-2 (in green) expression in the ischemic penumbra of the cortex. Nuclei were stained with DAPI and are visualised in blue. Scale bar = 50 μm. F Representative images of western blots for Nogo-A, NgR, and GAP-43. G Quantitative analysis of the western blot results. n = 4–6 per group. H-J Immunofluorescence staining was performed to show the presence of Nogo-A, NgR and β III tubulin in the ischemic penumbra of the cortex. Nuclei were stained with DAPI and are visualised in blue. Scale bar =, 50 μm. The data are presented as the means ± SEM. *P 
2). Electroacupuncture treatment improves motor function and neurological outcomes after cerebral ischemia/reperfusion injury. Neural Regeneration Research, 2022 (PubMed: 34916440) [IF=6.1]

Application: WB    Species: Rat    Sample:

Figure 5 EA promotes the repair of myelin in the ischemic penumbra and inhibits the expression of Nogo-A and NgR 7 days after MCAO/R.EA treatment was performed at the LI11 and ST36 acupoints in MCAO/R rats. ANA-12 was delivered via intraperitoneal injection at 0.5 mg/kg once per day for 7 consecutive days. (A) Representative images of Luxol fast blue staining at 7 days. There was a loss of myelin in destructive lesions post-MCAO/R, demyelination was significantly reduced after EA intervention, and the outcome in the MCAO/R + ANA-12 group was worse than that in the MCAO/R group. The arrow indicates the myelin in the ischemic penumbra. Scale bars: 1000 μm (upper) and 50 μm (lower). (B) Representative immunofluorescence images of Nogo-A (green, Alexa Fluor 488) in the ischemic penumbra. Nogo-A was significantly increased in the MCAO/R group compared with the sham group, and it could be reversed by EA treatment. Green: Nogo-A; blue: DAPI. Scale bars: 20 μm and 5 μm in the enlarged part. (C) The results of the immunofluorescence examination of NgR (green, Alexa Fluor 488) in the ischemic penumbra. Blue: DAPI. NgR expression was increased in the MCAO/R group, and significantly decreased after the EA intervention. Scale bars: 20 μm and 5 μm in the enlarged part. (D–F) EA inhibited the MCAO/R-induced protein expression of Nogo-A and NgR in the ischemic penumbra cortex, as determined by western blot. (G, H) Nogo-A and NgR mRNA expression levels were detected via quantitative real-time polymerase chain reaction. Data are presented as the mean ± SD (n = 6). ##P < 0.01, vs. sham group; *P < 0.05, **P < 0.01, vs. MCAO/R group; &&P < 0.01, vs. MCAO/R + EA group (one-way analysis of variance followed by least significant difference post hoc test). The experiments were repeated 3 times. ANA-12: TrkB inhibitor; DAPI: 4,6-diamidino-2-phenylindole; EA: electroacupuncture; MCAO/R: middle cerebral artery occlusion and reperfusion; NgR: Nogo receptor; TrkB: tyrosine kinase B.

Application: IF/ICC    Species: Rat    Sample:

Figure 5 EA promotes the repair of myelin in the ischemic penumbra and inhibits the expression of Nogo-A and NgR 7 days after MCAO/R.EA treatment was performed at the LI11 and ST36 acupoints in MCAO/R rats. ANA-12 was delivered via intraperitoneal injection at 0.5 mg/kg once per day for 7 consecutive days. (A) Representative images of Luxol fast blue staining at 7 days. There was a loss of myelin in destructive lesions post-MCAO/R, demyelination was significantly reduced after EA intervention, and the outcome in the MCAO/R + ANA-12 group was worse than that in the MCAO/R group. The arrow indicates the myelin in the ischemic penumbra. Scale bars: 1000 μm (upper) and 50 μm (lower). (B) Representative immunofluorescence images of Nogo-A (green, Alexa Fluor 488) in the ischemic penumbra. Nogo-A was significantly increased in the MCAO/R group compared with the sham group, and it could be reversed by EA treatment. Green: Nogo-A; blue: DAPI. Scale bars: 20 μm and 5 μm in the enlarged part. (C) The results of the immunofluorescence examination of NgR (green, Alexa Fluor 488) in the ischemic penumbra. Blue: DAPI. NgR expression was increased in the MCAO/R group, and significantly decreased after the EA intervention. Scale bars: 20 μm and 5 μm in the enlarged part. (D–F) EA inhibited the MCAO/R-induced protein expression of Nogo-A and NgR in the ischemic penumbra cortex, as determined by western blot. (G, H) Nogo-A and NgR mRNA expression levels were detected via quantitative real-time polymerase chain reaction. Data are presented as the mean ± SD (n = 6). ##P < 0.01, vs. sham group; *P < 0.05, **P < 0.01, vs. MCAO/R group; &&P < 0.01, vs. MCAO/R + EA group (one-way analysis of variance followed by least significant difference post hoc test). The experiments were repeated 3 times. ANA-12: TrkB inhibitor; DAPI: 4,6-diamidino-2-phenylindole; EA: electroacupuncture; MCAO/R: middle cerebral artery occlusion and reperfusion; NgR: Nogo receptor; TrkB: tyrosine kinase B.
3). Water Treadmill Training Ameliorates Neurite Outgrowth Inhibition Associated with NGR/RhoA/ROCK by Inhibiting Astrocyte Activation following Spinal Cord Injury. Oxidative Medicine and Cellular Longevity, 2021 (PubMed: 35387259)

Application: WB    Species: rat    Sample: T10 spinalcord

Figure 1:| TT decreased tissue structure damage and improved functional recovery after SCI. (a)–(j) Representative Western blots and quantification data for NF200/tubulin, GAP43/tubulin, GFAP/tubulin, Iba1/tubulin, CSPGs/GAPDH, NGR/GAPDH, RhoA/GAPDH,and ROCK2/CREB in each group.

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