antibody against β2 adrenergic receptors  (Alomone Labs)


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    Name:
    Anti beta2 Adrenergic Receptor extracellular Antibody
    Description:
    Anti β2 Adrenergic Receptor extracellular Antibody AAR 016 is a highly specific antibody directed against an extracellular epitope of the mouse β2 adrenoceptor The antibody can be used in western blot and immunohistochemistry applications It has been designed to recognize β2AR from mouse rat and human samples
    Catalog Number:
    AAR-016
    Price:
    397.0
    Category:
    Primary Antibody
    Applications:
    Immunohistochemistry, Western Blot
    Purity:
    Affinity purified on immobilized antigen.
    Immunogen:
    Synthetic peptide
    Size:
    25 mcl
    Antibody Type:
    Polyclonal Primary Antibodies
    Format:
    Lyophilized Powder
    Host:
    Rabbit
    Isotype:
    Rabbit IgG
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    Structured Review

    Alomone Labs antibody against β2 adrenergic receptors
    Anti beta2 Adrenergic Receptor extracellular Antibody
    Anti β2 Adrenergic Receptor extracellular Antibody AAR 016 is a highly specific antibody directed against an extracellular epitope of the mouse β2 adrenoceptor The antibody can be used in western blot and immunohistochemistry applications It has been designed to recognize β2AR from mouse rat and human samples
    https://www.bioz.com/result/antibody against β2 adrenergic receptors/product/Alomone Labs
    Average 94 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    antibody against β2 adrenergic receptors - by Bioz Stars, 2021-09
    94/100 stars

    Images

    1) Product Images from "Systemic administration of a β2-adrenergic receptor agonist reduces mechanical allodynia and suppresses the immune response to surgery in a rat model of persistent post-incisional hypersensitivity"

    Article Title: Systemic administration of a β2-adrenergic receptor agonist reduces mechanical allodynia and suppresses the immune response to surgery in a rat model of persistent post-incisional hypersensitivity

    Journal: Molecular Pain

    doi: 10.1177/1744806921997206

    Effects of β2 adrenergic receptor (AR) agonist on enhanced spinal microglia activation in a rat model of persistent postoperative pain. Sections of spinal cord were collected from rats 8 days following plantar incision and following treatment with DβH-saporin to deplete spinal noradrenergic terminals or control IgG-saporin. Rats were chronically administered clenbuterol (0.5 mg/kg, 2×/day, i.p.) or saline vehicle 6 days prior to and for 8 days after plantar incision. Depletion of spinal noradrenergic fibers was verified immunohistochemically with an antibody against dopamine β hydroxylase (DβH, (a)–(c)). Representative confocal images of IBA1-IR (blue, (d)–(f)) and phospho-p38 MAPK-IR (purple, (g)–(i)) in the ipsilateral spinal cord of incision rats. Localization of p38 MAPK in microglia was confirmed by colocalization with an antibody against the cell surface antigen CD11b (green, inset in (h)). Quantification of IBA1-IR in ipsilateral and contralateral spinal cord of rats with incision (j). Data represent mean ± SEM, n = 3 rats per group. Two way ANOVA indicated effect of group: p
    Figure Legend Snippet: Effects of β2 adrenergic receptor (AR) agonist on enhanced spinal microglia activation in a rat model of persistent postoperative pain. Sections of spinal cord were collected from rats 8 days following plantar incision and following treatment with DβH-saporin to deplete spinal noradrenergic terminals or control IgG-saporin. Rats were chronically administered clenbuterol (0.5 mg/kg, 2×/day, i.p.) or saline vehicle 6 days prior to and for 8 days after plantar incision. Depletion of spinal noradrenergic fibers was verified immunohistochemically with an antibody against dopamine β hydroxylase (DβH, (a)–(c)). Representative confocal images of IBA1-IR (blue, (d)–(f)) and phospho-p38 MAPK-IR (purple, (g)–(i)) in the ipsilateral spinal cord of incision rats. Localization of p38 MAPK in microglia was confirmed by colocalization with an antibody against the cell surface antigen CD11b (green, inset in (h)). Quantification of IBA1-IR in ipsilateral and contralateral spinal cord of rats with incision (j). Data represent mean ± SEM, n = 3 rats per group. Two way ANOVA indicated effect of group: p

    Techniques Used: Activation Assay

    Beta 2-adrenergic receptor immunoreactivity in the spinal cord of rats under naïve conditions and two days following plantar incision. Transverse section of L4 spinal cord of rat reacted with antibody against β2 adrenergic receptor ((a), β2-AR, green). There is a high density of immunoreactivity in cellular profiles throughout dorsal and ventral horn. There is also dense immunoreactivity in axon terminals within the lateral portion of the superficial laminae (arrow) and ependymal cells in the vicinity of the central canal (Arrowhead). Note lack of staining for β2-AR in motor neurons within the ventral horn (asterisk). Higher magnification confocal images show β2-AR-IR ((c), green) is present in a subpopulation of neurons ((d), NeuN, purple) in the dorsal spinal cord. Most β2-AR-IR cellular profiles colocalized with NeuN with the exception of a few non-neuronal profiles with morphology typical of microglia (arrows, (c)–(f)). β2-AR-IR non-neuronal cellular profiles in the spinal cord colocalized with the microglial marker IBA1 (red, (e) and (f)). Arrows in F indicate IBA1 negative neuronal cellular profiles. Representative images of β2 mRNA and DAPI in the dorsal spinal cord (g) with high power image showing colocalization with a subset of nuclei (h).
    Figure Legend Snippet: Beta 2-adrenergic receptor immunoreactivity in the spinal cord of rats under naïve conditions and two days following plantar incision. Transverse section of L4 spinal cord of rat reacted with antibody against β2 adrenergic receptor ((a), β2-AR, green). There is a high density of immunoreactivity in cellular profiles throughout dorsal and ventral horn. There is also dense immunoreactivity in axon terminals within the lateral portion of the superficial laminae (arrow) and ependymal cells in the vicinity of the central canal (Arrowhead). Note lack of staining for β2-AR in motor neurons within the ventral horn (asterisk). Higher magnification confocal images show β2-AR-IR ((c), green) is present in a subpopulation of neurons ((d), NeuN, purple) in the dorsal spinal cord. Most β2-AR-IR cellular profiles colocalized with NeuN with the exception of a few non-neuronal profiles with morphology typical of microglia (arrows, (c)–(f)). β2-AR-IR non-neuronal cellular profiles in the spinal cord colocalized with the microglial marker IBA1 (red, (e) and (f)). Arrows in F indicate IBA1 negative neuronal cellular profiles. Representative images of β2 mRNA and DAPI in the dorsal spinal cord (g) with high power image showing colocalization with a subset of nuclei (h).

    Techniques Used: Staining, Marker

    β2-adrenergic receptor immunoreactivity (β2AR-IR) in hindpaw of rats under naïve conditions and following plantar incision. Skin sections were obtained from the hind paw of naïve rats and incision rats two days following surgery. Sixteen-μm-thick sections were stained with antibodies against β2AR-IR (green, (a)–(c)), IBA1 (red, (d)–(f)) to label all monocytes/and macrophage, CD68 (blue, (g)–(i)) for activated M1 macrophage) and DAPI ((j) and (k)) to label all nuclei. β2-AR IR was present in keratinocytes of both naïve and incision rats. Two days following plantar incision there were increased β2-AR IR cellular profiles in predominantly the dermal layers of the skin. Higher magnification confocal images ((c), (f), (i), and (l)) indicate colocalization of β2-AR in IBA1 + cells and a subset of which express CD68-IR. Note in naïve skin IBA1-IR was primarily present at the epidermal/dermal interface and had reduced dermal cellularity (DAPI + cells) compared to skin adjacent to the wound in incision rats.
    Figure Legend Snippet: β2-adrenergic receptor immunoreactivity (β2AR-IR) in hindpaw of rats under naïve conditions and following plantar incision. Skin sections were obtained from the hind paw of naïve rats and incision rats two days following surgery. Sixteen-μm-thick sections were stained with antibodies against β2AR-IR (green, (a)–(c)), IBA1 (red, (d)–(f)) to label all monocytes/and macrophage, CD68 (blue, (g)–(i)) for activated M1 macrophage) and DAPI ((j) and (k)) to label all nuclei. β2-AR IR was present in keratinocytes of both naïve and incision rats. Two days following plantar incision there were increased β2-AR IR cellular profiles in predominantly the dermal layers of the skin. Higher magnification confocal images ((c), (f), (i), and (l)) indicate colocalization of β2-AR in IBA1 + cells and a subset of which express CD68-IR. Note in naïve skin IBA1-IR was primarily present at the epidermal/dermal interface and had reduced dermal cellularity (DAPI + cells) compared to skin adjacent to the wound in incision rats.

    Techniques Used: Staining

    Related Articles

    Incubation:

    Article Title: β3 Adrenoceptor‐induced cholinergic inhibition in human and rat urinary bladders involves the exchange protein directly activated by cyclic AMP 1 favoring adenosine release, et al. β3 Adrenoceptor‐induced cholinergic inhibition in human and rat urinary bladders involves the exchange protein directly activated by cyclic AMP 1 favoring adenosine release
    Article Snippet: .. The membranes were, then, blocked in Tris‐buffered saline (in mM: Tris–HCl 10 [pH 7.6], NaCl 150) containing Tween 20 0.05% and BSA 5% and, subsequently, incubated either with the following primary antibodies: rabbit anti‐β2 (AAR‐016; 1:200) and anti‐β3 (AAR‐017; 1:200) adrenoceptor primary antibodies from Alomone Labs (Jerusalem, Israel) or with rabbit anti‐EPAC1 (ab21236; 1:100; Abcam, Cambridge, UK) and mouse anti‐EPAC2 (5B1, mAb #4156; 1:500; Cell Signaling Technology, Danvers, MA, USA), in the above blocking buffer overnight at 4°C. ..

    Article Title: Differences in Noradrenaline Receptor Expression Across Different Neuronal Subtypes in Macaque Frontal Eye Field
    Article Snippet: .. Membranes were blocked with Intercept Blocking Buffer (LiCor 927-70001) and then incubated overnight with anti-α1A adrenergic receptor (Alomone Labs AAR-015), anti-α2A adrenergic receptor (Alomone Labs AAR-020), anti-β1 adrenergic receptor (Alomone Labs AAR-023), or anti-β2 adrenergic receptor (Alomone Labs AAR-016) pre-incubated with peptide plus 1% BSA, or pre-incubated with 1% BSA alone. ..

    Blocking Assay:

    Article Title: β3 Adrenoceptor‐induced cholinergic inhibition in human and rat urinary bladders involves the exchange protein directly activated by cyclic AMP 1 favoring adenosine release, et al. β3 Adrenoceptor‐induced cholinergic inhibition in human and rat urinary bladders involves the exchange protein directly activated by cyclic AMP 1 favoring adenosine release
    Article Snippet: .. The membranes were, then, blocked in Tris‐buffered saline (in mM: Tris–HCl 10 [pH 7.6], NaCl 150) containing Tween 20 0.05% and BSA 5% and, subsequently, incubated either with the following primary antibodies: rabbit anti‐β2 (AAR‐016; 1:200) and anti‐β3 (AAR‐017; 1:200) adrenoceptor primary antibodies from Alomone Labs (Jerusalem, Israel) or with rabbit anti‐EPAC1 (ab21236; 1:100; Abcam, Cambridge, UK) and mouse anti‐EPAC2 (5B1, mAb #4156; 1:500; Cell Signaling Technology, Danvers, MA, USA), in the above blocking buffer overnight at 4°C. ..

    Article Title: Differences in Noradrenaline Receptor Expression Across Different Neuronal Subtypes in Macaque Frontal Eye Field
    Article Snippet: .. Membranes were blocked with Intercept Blocking Buffer (LiCor 927-70001) and then incubated overnight with anti-α1A adrenergic receptor (Alomone Labs AAR-015), anti-α2A adrenergic receptor (Alomone Labs AAR-020), anti-β1 adrenergic receptor (Alomone Labs AAR-023), or anti-β2 adrenergic receptor (Alomone Labs AAR-016) pre-incubated with peptide plus 1% BSA, or pre-incubated with 1% BSA alone. ..

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    Alomone Labs antibody against β2 adrenergic receptors
    Effects of <t>β2</t> adrenergic receptor (AR) agonist on enhanced spinal microglia activation in a rat model of persistent postoperative pain. Sections of spinal cord were collected from rats 8 days following plantar incision and following treatment with DβH-saporin to deplete spinal noradrenergic terminals or control IgG-saporin. Rats were chronically administered clenbuterol (0.5 mg/kg, 2×/day, i.p.) or saline vehicle 6 days prior to and for 8 days after plantar incision. Depletion of spinal noradrenergic fibers was verified immunohistochemically with an antibody against dopamine β hydroxylase (DβH, (a)–(c)). Representative confocal images of IBA1-IR (blue, (d)–(f)) and phospho-p38 MAPK-IR (purple, (g)–(i)) in the ipsilateral spinal cord of incision rats. Localization of p38 MAPK in microglia was confirmed by colocalization with an antibody against the cell surface antigen CD11b (green, inset in (h)). Quantification of IBA1-IR in ipsilateral and contralateral spinal cord of rats with incision (j). Data represent mean ± SEM, n = 3 rats per group. Two way ANOVA indicated effect of group: p
    Antibody Against β2 Adrenergic Receptors, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/antibody against β2 adrenergic receptors/product/Alomone Labs
    Average 94 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    antibody against β2 adrenergic receptors - by Bioz Stars, 2021-09
    94/100 stars
      Buy from Supplier

    88
    Alomone Labs rabbit polyclonal anti nav1 8
    Effects of <t>β2</t> adrenergic receptor (AR) agonist on enhanced spinal microglia activation in a rat model of persistent postoperative pain. Sections of spinal cord were collected from rats 8 days following plantar incision and following treatment with DβH-saporin to deplete spinal noradrenergic terminals or control IgG-saporin. Rats were chronically administered clenbuterol (0.5 mg/kg, 2×/day, i.p.) or saline vehicle 6 days prior to and for 8 days after plantar incision. Depletion of spinal noradrenergic fibers was verified immunohistochemically with an antibody against dopamine β hydroxylase (DβH, (a)–(c)). Representative confocal images of IBA1-IR (blue, (d)–(f)) and phospho-p38 MAPK-IR (purple, (g)–(i)) in the ipsilateral spinal cord of incision rats. Localization of p38 MAPK in microglia was confirmed by colocalization with an antibody against the cell surface antigen CD11b (green, inset in (h)). Quantification of IBA1-IR in ipsilateral and contralateral spinal cord of rats with incision (j). Data represent mean ± SEM, n = 3 rats per group. Two way ANOVA indicated effect of group: p
    Rabbit Polyclonal Anti Nav1 8, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 88/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/rabbit polyclonal anti nav1 8/product/Alomone Labs
    Average 88 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    rabbit polyclonal anti nav1 8 - by Bioz Stars, 2021-09
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    Effects of β2 adrenergic receptor (AR) agonist on enhanced spinal microglia activation in a rat model of persistent postoperative pain. Sections of spinal cord were collected from rats 8 days following plantar incision and following treatment with DβH-saporin to deplete spinal noradrenergic terminals or control IgG-saporin. Rats were chronically administered clenbuterol (0.5 mg/kg, 2×/day, i.p.) or saline vehicle 6 days prior to and for 8 days after plantar incision. Depletion of spinal noradrenergic fibers was verified immunohistochemically with an antibody against dopamine β hydroxylase (DβH, (a)–(c)). Representative confocal images of IBA1-IR (blue, (d)–(f)) and phospho-p38 MAPK-IR (purple, (g)–(i)) in the ipsilateral spinal cord of incision rats. Localization of p38 MAPK in microglia was confirmed by colocalization with an antibody against the cell surface antigen CD11b (green, inset in (h)). Quantification of IBA1-IR in ipsilateral and contralateral spinal cord of rats with incision (j). Data represent mean ± SEM, n = 3 rats per group. Two way ANOVA indicated effect of group: p

    Journal: Molecular Pain

    Article Title: Systemic administration of a β2-adrenergic receptor agonist reduces mechanical allodynia and suppresses the immune response to surgery in a rat model of persistent post-incisional hypersensitivity

    doi: 10.1177/1744806921997206

    Figure Lengend Snippet: Effects of β2 adrenergic receptor (AR) agonist on enhanced spinal microglia activation in a rat model of persistent postoperative pain. Sections of spinal cord were collected from rats 8 days following plantar incision and following treatment with DβH-saporin to deplete spinal noradrenergic terminals or control IgG-saporin. Rats were chronically administered clenbuterol (0.5 mg/kg, 2×/day, i.p.) or saline vehicle 6 days prior to and for 8 days after plantar incision. Depletion of spinal noradrenergic fibers was verified immunohistochemically with an antibody against dopamine β hydroxylase (DβH, (a)–(c)). Representative confocal images of IBA1-IR (blue, (d)–(f)) and phospho-p38 MAPK-IR (purple, (g)–(i)) in the ipsilateral spinal cord of incision rats. Localization of p38 MAPK in microglia was confirmed by colocalization with an antibody against the cell surface antigen CD11b (green, inset in (h)). Quantification of IBA1-IR in ipsilateral and contralateral spinal cord of rats with incision (j). Data represent mean ± SEM, n = 3 rats per group. Two way ANOVA indicated effect of group: p

    Article Snippet: We used a previously characterized antibody against β2 adrenergic receptors (AAR-016, β2-AR, 1:1000, rabbit anti-mouse, Alomone Labs; Jerusalem, Israel).

    Techniques: Activation Assay

    Beta 2-adrenergic receptor immunoreactivity in the spinal cord of rats under naïve conditions and two days following plantar incision. Transverse section of L4 spinal cord of rat reacted with antibody against β2 adrenergic receptor ((a), β2-AR, green). There is a high density of immunoreactivity in cellular profiles throughout dorsal and ventral horn. There is also dense immunoreactivity in axon terminals within the lateral portion of the superficial laminae (arrow) and ependymal cells in the vicinity of the central canal (Arrowhead). Note lack of staining for β2-AR in motor neurons within the ventral horn (asterisk). Higher magnification confocal images show β2-AR-IR ((c), green) is present in a subpopulation of neurons ((d), NeuN, purple) in the dorsal spinal cord. Most β2-AR-IR cellular profiles colocalized with NeuN with the exception of a few non-neuronal profiles with morphology typical of microglia (arrows, (c)–(f)). β2-AR-IR non-neuronal cellular profiles in the spinal cord colocalized with the microglial marker IBA1 (red, (e) and (f)). Arrows in F indicate IBA1 negative neuronal cellular profiles. Representative images of β2 mRNA and DAPI in the dorsal spinal cord (g) with high power image showing colocalization with a subset of nuclei (h).

    Journal: Molecular Pain

    Article Title: Systemic administration of a β2-adrenergic receptor agonist reduces mechanical allodynia and suppresses the immune response to surgery in a rat model of persistent post-incisional hypersensitivity

    doi: 10.1177/1744806921997206

    Figure Lengend Snippet: Beta 2-adrenergic receptor immunoreactivity in the spinal cord of rats under naïve conditions and two days following plantar incision. Transverse section of L4 spinal cord of rat reacted with antibody against β2 adrenergic receptor ((a), β2-AR, green). There is a high density of immunoreactivity in cellular profiles throughout dorsal and ventral horn. There is also dense immunoreactivity in axon terminals within the lateral portion of the superficial laminae (arrow) and ependymal cells in the vicinity of the central canal (Arrowhead). Note lack of staining for β2-AR in motor neurons within the ventral horn (asterisk). Higher magnification confocal images show β2-AR-IR ((c), green) is present in a subpopulation of neurons ((d), NeuN, purple) in the dorsal spinal cord. Most β2-AR-IR cellular profiles colocalized with NeuN with the exception of a few non-neuronal profiles with morphology typical of microglia (arrows, (c)–(f)). β2-AR-IR non-neuronal cellular profiles in the spinal cord colocalized with the microglial marker IBA1 (red, (e) and (f)). Arrows in F indicate IBA1 negative neuronal cellular profiles. Representative images of β2 mRNA and DAPI in the dorsal spinal cord (g) with high power image showing colocalization with a subset of nuclei (h).

    Article Snippet: We used a previously characterized antibody against β2 adrenergic receptors (AAR-016, β2-AR, 1:1000, rabbit anti-mouse, Alomone Labs; Jerusalem, Israel).

    Techniques: Staining, Marker

    β2-adrenergic receptor immunoreactivity (β2AR-IR) in hindpaw of rats under naïve conditions and following plantar incision. Skin sections were obtained from the hind paw of naïve rats and incision rats two days following surgery. Sixteen-μm-thick sections were stained with antibodies against β2AR-IR (green, (a)–(c)), IBA1 (red, (d)–(f)) to label all monocytes/and macrophage, CD68 (blue, (g)–(i)) for activated M1 macrophage) and DAPI ((j) and (k)) to label all nuclei. β2-AR IR was present in keratinocytes of both naïve and incision rats. Two days following plantar incision there were increased β2-AR IR cellular profiles in predominantly the dermal layers of the skin. Higher magnification confocal images ((c), (f), (i), and (l)) indicate colocalization of β2-AR in IBA1 + cells and a subset of which express CD68-IR. Note in naïve skin IBA1-IR was primarily present at the epidermal/dermal interface and had reduced dermal cellularity (DAPI + cells) compared to skin adjacent to the wound in incision rats.

    Journal: Molecular Pain

    Article Title: Systemic administration of a β2-adrenergic receptor agonist reduces mechanical allodynia and suppresses the immune response to surgery in a rat model of persistent post-incisional hypersensitivity

    doi: 10.1177/1744806921997206

    Figure Lengend Snippet: β2-adrenergic receptor immunoreactivity (β2AR-IR) in hindpaw of rats under naïve conditions and following plantar incision. Skin sections were obtained from the hind paw of naïve rats and incision rats two days following surgery. Sixteen-μm-thick sections were stained with antibodies against β2AR-IR (green, (a)–(c)), IBA1 (red, (d)–(f)) to label all monocytes/and macrophage, CD68 (blue, (g)–(i)) for activated M1 macrophage) and DAPI ((j) and (k)) to label all nuclei. β2-AR IR was present in keratinocytes of both naïve and incision rats. Two days following plantar incision there were increased β2-AR IR cellular profiles in predominantly the dermal layers of the skin. Higher magnification confocal images ((c), (f), (i), and (l)) indicate colocalization of β2-AR in IBA1 + cells and a subset of which express CD68-IR. Note in naïve skin IBA1-IR was primarily present at the epidermal/dermal interface and had reduced dermal cellularity (DAPI + cells) compared to skin adjacent to the wound in incision rats.

    Article Snippet: We used a previously characterized antibody against β2 adrenergic receptors (AAR-016, β2-AR, 1:1000, rabbit anti-mouse, Alomone Labs; Jerusalem, Israel).

    Techniques: Staining