Product: Nogo A Antibody
Catalog: DF8581
Description: Rabbit polyclonal antibody to Nogo A
Application: WB IHC
Reactivity: Human, Mouse, Rat
Prediction: Pig, Horse, Rabbit
Mol.Wt.: 129 kDa; 130kD(Calculated).
Uniprot: Q9NQC3
RRID: AB_2841785

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Product Info

Source:
Rabbit
Application:
WB 1:1000-3000, IHC 1:50-200
*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(100%), Horse(100%), Rabbit(100%)
Clonality:
Polyclonal
Specificity:
Nogo A Antibody detects endogenous levels of total Nogo A.
RRID:
AB_2841785
Cite Format: Affinity Biosciences Cat# DF8581, RRID:AB_2841785.
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

1110020G17Rik; AA407876; AA409940; AA960376; ASY; C130026I10Rik; Foocen; Glut4 vesicle 20 kDa protein; Human NogoA; Kiaa0886; KIAA4153; MGC116054; MGC139261; mKIAA0886; mKIAA4153; My043 protein; Nbla00271; Nbla10545; Neurite growth inhibitor 220; Neurite Growth Inhibitor 220, included; Neurite outgrowth inhibitor; Neuroendocrine-specific protein; Neuroendocrine-specific protein C homolog; NI-250; NI220/250; Nogo A; NOGO; Nogo B; Nogo C; Nogo protein; NOGOC; NSP; NSP-CL; rat N; Reticulon 4; Reticulon 5; Reticulon-4; Reticulon-5; RTN X; RTN-x; Rtn4; Rtn4 reticulon 4; RTN4-A; RTN4-B1; RTN4-B2; RTN4-C; RTN4_HUMAN; Vp20;

Immunogens

Immunogen:
Uniprot:
Gene(ID):
Expression:
Q9NQC3 RTN4_HUMAN:

Isoform A: is specifically expressed in brain and testis and weakly in heart and skeletal muscle. Isoform B: widely expressed except for the liver. Highly expressed in endothelial cells and vascular smooth muscle cells, including blood vessels and mesenteric arteries (PubMed:15034570, PubMed:21183689). Isoform C: is expressed in brain, skeletal muscle and adipocytes. Isoform D is testis-specific.

Sequence:
MEDLDQSPLVSSSDSPPRPQPAFKYQFVREPEDEEEEEEEEEEDEDEDLEELEVLERKPAAGLSAAPVPTAPAAGAPLMDFGNDFVPPAPRGPLPAAPPVAPERQPSWDPSPVSSTVPAPSPLSAAAVSPSKLPEDDEPPARPPPPPPASVSPQAEPVWTPPAPAPAAPPSTPAAPKRRGSSGSVDETLFALPAASEPVIRSSAENMDLKEQPGNTISAGQEDFPSVLLETAASLPSLSPLSAASFKEHEYLGNLSTVLPTEGTLQENVSEASKEVSEKAKTLLIDRDLTEFSELEYSEMGSSFSVSPKAESAVIVANPREEIIVKNKDEEEKLVSNNILHNQQELPTALTKLVKEDEVVSSEKAKDSFNEKRVAVEAPMREEYADFKPFERVWEVKDSKEDSDMLAAGGKIESNLESKVDKKCFADSLEQTNHEKDSESSNDDTSFPSTPEGIKDRSGAYITCAPFNPAATESIATNIFPLLGDPTSENKTDEKKIEEKKAQIVTEKNTSTKTSNPFLVAAQDSETDYVTTDNLTKVTEEVVANMPEGLTPDLVQEACESELNEVTGTKIAYETKMDLVQTSEVMQESLYPAAQLCPSFEESEATPSPVLPDIVMEAPLNSAVPSAGASVIQPSSSPLEASSVNYESIKHEPENPPPYEEAMSVSLKKVSGIKEEIKEPENINAALQETEAPYISIACDLIKETKLSAEPAPDFSDYSEMAKVEQPVPDHSELVEDSSPDSEPVDLFSDDSIPDVPQKQDETVMLVKESLTETSFESMIEYENKEKLSALPPEGGKPYLESFKLSLDNTKDTLLPDEVSTLSKKEKIPLQMEELSTAVYSNDDLFISKEAQIRETETFSDSSPIEIIDEFPTLISSKTDSFSKLAREYTDLEVSHKSEIANAPDGAGSLPCTELPHDLSLKNIQPKVEEKISFSDDFSKNGSATSKVLLLPPDVSALATQAEIESIVKPKVLVKEAEKKLPSDTEKEDRSPSAIFSAELSKTSVVDLLYWRDIKKTGVVFGASLFLLLSLTVFSIVSVTAYIALALLSVTISFRIYKGVIQAIQKSDEGHPFRAYLESEVAISEELVQKYSNSALGHVNCTIKELRRLFLVDDLVDSLKFAVLMWVFTYVGALFNGLTLLILALISLFSVPVIYERHQAQIDHYLGLANKNVKDAMAKIQAKIPGLKRKAE

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
100
Horse
100
Rabbit
100
Bovine
0
Sheep
0
Dog
0
Xenopus
0
Zebrafish
0
Chicken
0
Model Confidence:
High(score>80) Medium(80>score>50) Low(score<50) No confidence

PTMs - Q9NQC3 As Substrate

Site PTM Type Enzyme
M1 Acetylation
S7 Phosphorylation
S11 Phosphorylation
S12 Phosphorylation
S13 Phosphorylation
S15 Phosphorylation
Y25 Phosphorylation
K58 Ubiquitination
S107 Phosphorylation P49137 (MAPKAPK2)
S111 Phosphorylation
S114 Phosphorylation
S115 Phosphorylation
T116 Phosphorylation
S121 Phosphorylation
S124 Phosphorylation
S129 Phosphorylation
S152 Phosphorylation
T160 Phosphorylation
T172 Phosphorylation P28482 (MAPK1)
S181 Phosphorylation
S182 Phosphorylation
S184 Phosphorylation
T188 Phosphorylation
S234 Phosphorylation
T282 Phosphorylation
Y384 Phosphorylation
S418 Phosphorylation
T450 Phosphorylation
S515 Phosphorylation
S525 Phosphorylation
Y529 Phosphorylation
Y646 Phosphorylation
Y659 Phosphorylation
K674 Ubiquitination
Y694 Phosphorylation P06241 (FYN)
Y718 Phosphorylation
T763 Phosphorylation
S778 Phosphorylation
Y782 Phosphorylation
S823 Phosphorylation
Y840 Phosphorylation
S863 Phosphorylation
S876 Phosphorylation
T879 Phosphorylation
S881 Phosphorylation
K884 Ubiquitination
Y889 Phosphorylation
S920 Phosphorylation
S943 Phosphorylation
T945 Phosphorylation
S946 Phosphorylation
S991 Phosphorylation
S993 Phosphorylation
K1002 Ubiquitination
K1066 Ubiquitination
K1090 Ubiquitination
C1101 S-Nitrosylation
K1104 Acetylation
K1104 Ubiquitination
Y1165 Phosphorylation
K1171 Ubiquitination
K1174 Ubiquitination
K1179 Ubiquitination
K1183 Ubiquitination

Research Backgrounds

Function:

Required to induce the formation and stabilization of endoplasmic reticulum (ER) tubules. They regulate membrane morphogenesis in the ER by promoting tubular ER production. They influence nuclear envelope expansion, nuclear pore complex formation and proper localization of inner nuclear membrane proteins. However each isoform have specific functions mainly depending on their tissue expression specificities (Probable).

Developmental neurite growth regulatory factor with a role as a negative regulator of axon-axon adhesion and growth, and as a facilitator of neurite branching. Regulates neurite fasciculation, branching and extension in the developing nervous system. Involved in down-regulation of growth, stabilization of wiring and restriction of plasticity in the adult CNS. Regulates the radial migration of cortical neurons via an RTN4R-LINGO1 containing receptor complex (By similarity). Acts as a negative regulator of central nervous system angiogenesis. Inhibits spreading, migration and sprouting of primary brain microvascular endothelial cells (MVECs). Also induces the retraction of MVECs lamellipodia and filopodia in a ROCK pathway-dependent manner (By similarity).

Mainly function in endothelial cells and vascular smooth muscle cells, is also involved in immune system regulation (Probable). Modulator of vascular remodeling, promotes the migration of endothelial cells but inhibits the migration of vascular smooth muscle cells. Regulates endothelial sphingolipid biosynthesis with direct effects on vascular function and blood pressure. Inhibits serine palmitoyltransferase, SPTLC1, the rate-limiting enzyme of the novo sphingolipid biosynthetic pathway, thereby controlling production of endothelial sphingosine-1-phosphate (S1P). Required to promote macrophage homing and functions such as cytokine/chemokine gene expression involved in angiogenesis, arteriogenesis and tissue repair. Mediates ICAM1 induced transendothelial migration of leukocytes such as monocytes and neutrophils and acute inflammation. Necessary for immune responses triggered by nucleic acid sensing TLRs, such as TLR9, is required for proper TLR9 location to endolysosomes. Also involved in immune response to LPS. Plays a role in liver regeneration through the modulation of hepatocytes proliferation (By similarity). Reduces the anti-apoptotic activity of Bcl-xl and Bcl-2. This is likely consecutive to their change in subcellular location, from the mitochondria to the endoplasmic reticulum, after binding and sequestration. With isoform C, inhibits BACE1 activity and amyloid precursor protein processing.

Regulates cardiomyocyte apoptosis upon hypoxic conditions (By similarity). With isoform B, inhibits BACE1 activity and amyloid precursor protein processing.

Subcellular Location:

Endoplasmic reticulum membrane>Multi-pass membrane protein. Cell membrane>Multi-pass membrane protein>Cytoplasmic side.
Note: Anchored to the membrane of the endoplasmic reticulum (ER) through 2 putative transmembrane domains. Localizes throughout the ER tubular network (PubMed:27619977). Co-localizes with TMEM33 at the ER sheets.

Endoplasmic reticulum membrane>Multi-pass membrane protein. Cell membrane>Multi-pass membrane protein>Extracellular side. Cell junction.
Note: Mainly located on endoplasmic reticulum tubules and sheet edges (PubMed:27786289). Upon ICAM1 engagement, redistributed toward endothelial junctions where interacts with CDH5 (PubMed:21183689).

Endoplasmic reticulum membrane>Multi-pass membrane protein.

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

Isoform A: is specifically expressed in brain and testis and weakly in heart and skeletal muscle. Isoform B: widely expressed except for the liver. Highly expressed in endothelial cells and vascular smooth muscle cells, including blood vessels and mesenteric arteries. Isoform C: is expressed in brain, skeletal muscle and adipocytes. Isoform D is testis-specific.

Subunit Structure:

Binds to RTN4R. Interacts with ATL1. Interacts with TMEM170A. Interacts with RTN4IP1 (By similarity). Isoform A: interacts in trans with CNTNAP1 (By similarity). Isoform B: homodimerizes. Isoform B: interacts with BAD/Bcl-xl and BCL2. Isoform B: binds to NGBR and RTN3. Isoform B: interacts with SPTLC1 (By similarity). Isoform B: interacts with GRAMD4 (By similarity). Isoform B: interacts with CDH5. Isoform B: interacts with BACE1 and BACE2. Isoform C: interacts with BACE1 and BACE2. Isoform C: interacts with TMEM33.

Family&Domains:

Three regions, residues 59-172, 544-725 and the loop 66 amino acids, between the two transmembrane domains, known as Nogo-66 loop, appear to be responsible for the inhibitory effect on neurite outgrowth and the spreading of neurons. This Nogo-66 loop, mediates also the binding of RTN4 to its receptor (By similarity).

N-terminal part, called Am-Nogo-B(1-200), is the functional domain for RTN4B-mediated signaling in endothelial and vascular smooth muscle cells.

Research Fields

· Human Diseases > Neurodegenerative diseases > Alzheimer's disease.

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.

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