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Product listing: IFN-β1 (D2J1D) Rabbit mAb (Mouse Specific), UniProt ID P01575 #97450 to IL-1RA (20D8) Mouse mAb, UniProt ID P18510 #3865

$260
100 µl
APPLICATIONS
REACTIVITY
Mouse

Application Methods: Flow Cytometry, Western Blotting

Background: The type I interferon (IFN) family includes IFN-β1 and IFN-α1 through IFN-α13 in humans and IFN-α1 through IFN-α14 in mice. Type I IFN is produced following detection of pathogen-associated molecular patterns (PAMPs) and is important for induction of antiviral genes, activation of dendritic cells, and initiation of adaptive immunity (1, 2). Type I IFNs signal through the IFN alpha receptor (IFNAR), which is a heterodimer composed of IFNAR1 and IFNAR2. Activation of IFNAR leads to formation of the nuclear complex IFN-stimulated gene factor 3 (ISGF3), which consists of STAT1, STAT2, and IRF-9 (3, 4). ISGF3 binds to IFN-stimulated response elements (ISREs) to initiate transcription of interferon-stimulated genes (3).

$260
100 µl
APPLICATIONS
REACTIVITY
Human

Application Methods: Immunoprecipitation, Peptide ELISA (DELFIA), Western Blotting

Background: IFN-γ plays key roles in both the innate and adaptive immune response. IFN-γ activates the cytotoxic activity of innate immune cells, such as macrophages and NK cells (1,2). IFN-γ production by NK cells and antigen presenting cells (APCs) promotes cell-mediated adaptive immunity by inducing IFN-γ production by T lymphocytes, increasing class I and class II MHC expression, and enhancing peptide antigen presentation (1). The anti-viral activity of IFN-γ is due to its induction of PKR and other regulatory proteins. Binding of IFN-γ to the IFNGR1/IFNGR2 complex promotes dimerization of the receptor complexes to form the (IFNGR1/IFNGR2)2 -IFN-γ dimer. Binding induces a conformational change in receptor intracellular domains and signaling involves Jak1, Jak2, and Stat1 (3). The critical role of IFN-γ in amplification of immune surveillance and function is supported by increased susceptibility to pathogen infection by IFN-γ or IFNGR knockout mice and in humans with inactivating mutations in IFNGR1 or IFNGR2. IFN-γ also appears to have a role in atherosclerosis (4).

$348
50 tests
100 µl
This Cell Signaling Technology antibody is conjugated to Alexa Fluor® 488 fluorescent dye and tested in-house for direct flow cytometry analysis in human cells. This antibody is expected to exhibit the same species cross-reactivity as the unconjugated IFN-γ (D3H2) XP® Rabbit mAb #8455.
APPLICATIONS
REACTIVITY
Human

Application Methods: Flow Cytometry

Background: IFN-γ plays key roles in both the innate and adaptive immune response. IFN-γ activates the cytotoxic activity of innate immune cells, such as macrophages and NK cells (1,2). IFN-γ production by NK cells and antigen presenting cells (APCs) promotes cell-mediated adaptive immunity by inducing IFN-γ production by T lymphocytes, increasing class I and class II MHC expression, and enhancing peptide antigen presentation (1). The anti-viral activity of IFN-γ is due to its induction of PKR and other regulatory proteins. Binding of IFN-γ to the IFNGR1/IFNGR2 complex promotes dimerization of the receptor complexes to form the (IFNGR1/IFNGR2)2 -IFN-γ dimer. Binding induces a conformational change in receptor intracellular domains and signaling involves Jak1, Jak2, and Stat1 (3). The critical role of IFN-γ in amplification of immune surveillance and function is supported by increased susceptibility to pathogen infection by IFN-γ or IFNGR knockout mice and in humans with inactivating mutations in IFNGR1 or IFNGR2. IFN-γ also appears to have a role in atherosclerosis (4).

$348
50 tests
100 µl
This Cell Signaling Technology antibody is conjugated to Alexa Fluor® 647 fluorescent dye and tested in-house for direct flow cytometry analysis in human cells. This antibody is expected to exhibit the same species cross-reactivity as the unconjugated IFN-γ (D3H2) XP® Rabbit mAb #8455.
APPLICATIONS
REACTIVITY
Human

Application Methods: Flow Cytometry

Background: IFN-γ plays key roles in both the innate and adaptive immune response. IFN-γ activates the cytotoxic activity of innate immune cells, such as macrophages and NK cells (1,2). IFN-γ production by NK cells and antigen presenting cells (APCs) promotes cell-mediated adaptive immunity by inducing IFN-γ production by T lymphocytes, increasing class I and class II MHC expression, and enhancing peptide antigen presentation (1). The anti-viral activity of IFN-γ is due to its induction of PKR and other regulatory proteins. Binding of IFN-γ to the IFNGR1/IFNGR2 complex promotes dimerization of the receptor complexes to form the (IFNGR1/IFNGR2)2 -IFN-γ dimer. Binding induces a conformational change in receptor intracellular domains and signaling involves Jak1, Jak2, and Stat1 (3). The critical role of IFN-γ in amplification of immune surveillance and function is supported by increased susceptibility to pathogen infection by IFN-γ or IFNGR knockout mice and in humans with inactivating mutations in IFNGR1 or IFNGR2. IFN-γ also appears to have a role in atherosclerosis (4).

$293
100 µl
APPLICATIONS
REACTIVITY
Human

Application Methods: Flow Cytometry, Immunofluorescence (Immunocytochemistry), Immunoprecipitation, Western Blotting

Background: IFN-γ plays key roles in both the innate and adaptive immune response. IFN-γ activates the cytotoxic activity of innate immune cells, such as macrophages and NK cells (1,2). IFN-γ production by NK cells and antigen presenting cells (APCs) promotes cell-mediated adaptive immunity by inducing IFN-γ production by T lymphocytes, increasing class I and class II MHC expression, and enhancing peptide antigen presentation (1). The anti-viral activity of IFN-γ is due to its induction of PKR and other regulatory proteins. Binding of IFN-γ to the IFNGR1/IFNGR2 complex promotes dimerization of the receptor complexes to form the (IFNGR1/IFNGR2)2 -IFN-γ dimer. Binding induces a conformational change in receptor intracellular domains and signaling involves Jak1, Jak2, and Stat1 (3). The critical role of IFN-γ in amplification of immune surveillance and function is supported by increased susceptibility to pathogen infection by IFN-γ or IFNGR knockout mice and in humans with inactivating mutations in IFNGR1 or IFNGR2. IFN-γ also appears to have a role in atherosclerosis (4).

$159
100 µg
This Cell Signaling Technology antibody is conjugated to APC and tested in-house for direct flow cytometric analysis in mouse cells.
APPLICATIONS
REACTIVITY
Mouse

Application Methods: Flow Cytometry

Background: IFN-γ plays key roles in both the innate and adaptive immune response. IFN-γ activates the cytotoxic activity of innate immune cells, such as macrophages and NK cells (1,2). IFN-γ production by NK cells and antigen presenting cells (APCs) promotes cell-mediated adaptive immunity by inducing IFN-γ production by T lymphocytes, increasing class I and class II MHC expression, and enhancing peptide antigen presentation (1). The anti-viral activity of IFN-γ is due to its induction of PKR and other regulatory proteins. Binding of IFN-γ to the IFNGR1/IFNGR2 complex promotes dimerization of the receptor complexes to form the (IFNGR1/IFNGR2)2 -IFN-γ dimer. Binding induces a conformational change in receptor intracellular domains and signaling involves Jak1, Jak2, and Stat1 (3). The critical role of IFN-γ in amplification of immune surveillance and function is supported by increased susceptibility to pathogen infection by IFN-γ or IFNGR knockout mice and in humans with inactivating mutations in IFNGR1 or IFNGR2. IFN-γ also appears to have a role in atherosclerosis (4).

$109
100 µg
This Cell Signaling Technology antibody is conjugated to FITC and tested in-house for direct flow cytometric analysis in mouse cells.
APPLICATIONS
REACTIVITY
Mouse

Application Methods: Flow Cytometry

Background: IFN-γ plays key roles in both the innate and adaptive immune response. IFN-γ activates the cytotoxic activity of innate immune cells, such as macrophages and NK cells (1,2). IFN-γ production by NK cells and antigen presenting cells (APCs) promotes cell-mediated adaptive immunity by inducing IFN-γ production by T lymphocytes, increasing class I and class II MHC expression, and enhancing peptide antigen presentation (1). The anti-viral activity of IFN-γ is due to its induction of PKR and other regulatory proteins. Binding of IFN-γ to the IFNGR1/IFNGR2 complex promotes dimerization of the receptor complexes to form the (IFNGR1/IFNGR2)2 -IFN-γ dimer. Binding induces a conformational change in receptor intracellular domains and signaling involves Jak1, Jak2, and Stat1 (3). The critical role of IFN-γ in amplification of immune surveillance and function is supported by increased susceptibility to pathogen infection by IFN-γ or IFNGR knockout mice and in humans with inactivating mutations in IFNGR1 or IFNGR2. IFN-γ also appears to have a role in atherosclerosis (4).

$129
100 µg
This Cell Signaling Technology antibody is conjugated to PE and tested in-house for direct flow cytometric analysis in mouse cells.
APPLICATIONS
REACTIVITY
Mouse

Application Methods: Flow Cytometry

Background: IFN-γ plays key roles in both the innate and adaptive immune response. IFN-γ activates the cytotoxic activity of innate immune cells, such as macrophages and NK cells (1,2). IFN-γ production by NK cells and antigen presenting cells (APCs) promotes cell-mediated adaptive immunity by inducing IFN-γ production by T lymphocytes, increasing class I and class II MHC expression, and enhancing peptide antigen presentation (1). The anti-viral activity of IFN-γ is due to its induction of PKR and other regulatory proteins. Binding of IFN-γ to the IFNGR1/IFNGR2 complex promotes dimerization of the receptor complexes to form the (IFNGR1/IFNGR2)2 -IFN-γ dimer. Binding induces a conformational change in receptor intracellular domains and signaling involves Jak1, Jak2, and Stat1 (3). The critical role of IFN-γ in amplification of immune surveillance and function is supported by increased susceptibility to pathogen infection by IFN-γ or IFNGR knockout mice and in humans with inactivating mutations in IFNGR1 or IFNGR2. IFN-γ also appears to have a role in atherosclerosis (4).

$260
100 µl
APPLICATIONS
REACTIVITY
Human, Monkey, Mouse, Rat

Application Methods: Immunoprecipitation, Western Blotting

$260
100 µl
APPLICATIONS
REACTIVITY
Human

Application Methods: Chromatin IP, Flow Cytometry, Immunofluorescence (Immunocytochemistry), Western Blotting

Background: The Ikaros family of zinc-finger DNA-binding proteins belongs to the Kruppel transcription factor superfamily. Ikaros proteins are characterized by the presence of an amino-terminal zinc finger DNA-binding domain and a carboxy-terminal dimerization domain. Members of the Ikaros family include Ikaros, Aiolos, Helios, EOS, and Pegasus (1). All family members can form homodimers and heterodimers with other members of the Ikaros family. Most also contain multiple isoforms that are generated as a result of differential splicing, with some isoforms behaving in a dominant negative manner upon dimerization (2).Ikaros (IKZF1, LYF1) is the prototypical Ikaros family zinc-finger transcription factor and is expressed abundantly in lymphoid cells. Genetic studies in mice demonstrate that Ikaros is a tumor suppressor that is important for the normal development of B, T, natural killer, and dendritic cells (3,4). Additional studies show that imbalanced expression of different Ikaros isoforms, as well as mutations in the corresponding IKAROS gene, can be associated with a number of hematologic malignancies in humans (2,5,6).

$305
50 tests
100 µl
This Cell Signaling Technology antibody is conjugated to Alexa Fluor® 488 fluorescent dye and tested in-house for direct flow cytometric analysis in human cells. This antibody is expected to exhibit the same species cross-reactivity as the unconjugated Ikaros (D6N9Y) Rabbit mAb #14859.
APPLICATIONS
REACTIVITY
Human, Mouse

Application Methods: Flow Cytometry

Background: The Ikaros family of zinc-finger DNA-binding proteins belongs to the Kruppel transcription factor superfamily. Ikaros proteins are characterized by the presence of an amino-terminal zinc finger DNA-binding domain and a carboxy-terminal dimerization domain. Members of the Ikaros family include Ikaros, Aiolos, Helios, EOS, and Pegasus (1). All family members can form homodimers and heterodimers with other members of the Ikaros family. Most also contain multiple isoforms that are generated as a result of differential splicing, with some isoforms behaving in a dominant negative manner upon dimerization (2).Ikaros (IKZF1, LYF1) is the prototypical Ikaros family zinc-finger transcription factor and is expressed abundantly in lymphoid cells. Genetic studies in mice demonstrate that Ikaros is a tumor suppressor that is important for the normal development of B, T, natural killer, and dendritic cells (3,4). Additional studies show that imbalanced expression of different Ikaros isoforms, as well as mutations in the corresponding IKAROS gene, can be associated with a number of hematologic malignancies in humans (2,5,6).

$305
50 tests
100 µl
This Cell Signaling Technology antibody is conjugated to Alexa Fluor® 647 fluorescent dye and tested in-house for direct flow cytometric analysis in human cells. This antibody is expected to exhibit the same species cross-reactivity as the unconjugated Ikaros (D6N9Y) Rabbit mAb #14859.
APPLICATIONS
REACTIVITY
Human, Mouse

Application Methods: Flow Cytometry

Background: The Ikaros family of zinc-finger DNA-binding proteins belongs to the Kruppel transcription factor superfamily. Ikaros proteins are characterized by the presence of an amino-terminal zinc finger DNA-binding domain and a carboxy-terminal dimerization domain. Members of the Ikaros family include Ikaros, Aiolos, Helios, EOS, and Pegasus (1). All family members can form homodimers and heterodimers with other members of the Ikaros family. Most also contain multiple isoforms that are generated as a result of differential splicing, with some isoforms behaving in a dominant negative manner upon dimerization (2).Ikaros (IKZF1, LYF1) is the prototypical Ikaros family zinc-finger transcription factor and is expressed abundantly in lymphoid cells. Genetic studies in mice demonstrate that Ikaros is a tumor suppressor that is important for the normal development of B, T, natural killer, and dendritic cells (3,4). Additional studies show that imbalanced expression of different Ikaros isoforms, as well as mutations in the corresponding IKAROS gene, can be associated with a number of hematologic malignancies in humans (2,5,6).

$305
50 tests
100 µl
This Cell Signaling Technology antibody is conjugated to phycoerythrin (PE) and tested in-house for direct flow cytometry analysis in human cells. This antibody is expected to exhibit the same species cross-reactivity as the unconjugated Ikaros (D6N9Y) Rabbit mAb #14859.
APPLICATIONS
REACTIVITY
Human, Mouse

Application Methods: Flow Cytometry

Background: The Ikaros family of zinc-finger DNA-binding proteins belongs to the Kruppel transcription factor superfamily. Ikaros proteins are characterized by the presence of an amino-terminal zinc finger DNA-binding domain and a carboxy-terminal dimerization domain. Members of the Ikaros family include Ikaros, Aiolos, Helios, EOS, and Pegasus (1). All family members can form homodimers and heterodimers with other members of the Ikaros family. Most also contain multiple isoforms that are generated as a result of differential splicing, with some isoforms behaving in a dominant negative manner upon dimerization (2).Ikaros (IKZF1, LYF1) is the prototypical Ikaros family zinc-finger transcription factor and is expressed abundantly in lymphoid cells. Genetic studies in mice demonstrate that Ikaros is a tumor suppressor that is important for the normal development of B, T, natural killer, and dendritic cells (3,4). Additional studies show that imbalanced expression of different Ikaros isoforms, as well as mutations in the corresponding IKAROS gene, can be associated with a number of hematologic malignancies in humans (2,5,6).

$260
100 µl
APPLICATIONS
REACTIVITY
Human, Mouse

Application Methods: Chromatin IP, Chromatin IP-seq, Flow Cytometry, Immunofluorescence (Immunocytochemistry), Immunohistochemistry (Paraffin), Western Blotting

Background: The Ikaros family of zinc-finger DNA-binding proteins belongs to the Kruppel transcription factor superfamily. Ikaros proteins are characterized by the presence of an amino-terminal zinc finger DNA-binding domain and a carboxy-terminal dimerization domain. Members of the Ikaros family include Ikaros, Aiolos, Helios, EOS, and Pegasus (1). All family members can form homodimers and heterodimers with other members of the Ikaros family. Most also contain multiple isoforms that are generated as a result of differential splicing, with some isoforms behaving in a dominant negative manner upon dimerization (2).Ikaros (IKZF1, LYF1) is the prototypical Ikaros family zinc-finger transcription factor and is expressed abundantly in lymphoid cells. Genetic studies in mice demonstrate that Ikaros is a tumor suppressor that is important for the normal development of B, T, natural killer, and dendritic cells (3,4). Additional studies show that imbalanced expression of different Ikaros isoforms, as well as mutations in the corresponding IKAROS gene, can be associated with a number of hematologic malignancies in humans (2,5,6).

$305
50 tests
100 µl
This Cell Signaling Technology antibody is conjugated to phycoerythrin (PE) and tested in-house for direct flow cytometry analysis in human cells. This antibody is expected to exhibit the same species cross-reactivity as the unconjugated IKKα (3G12) Mouse mAb #11930.
APPLICATIONS
REACTIVITY
Human, Monkey

Application Methods: Flow Cytometry

Background: The NF-κB/Rel transcription factors are present in the cytosol in an inactive state, complexed with the inhibitory IκB proteins (1-3). Most agents that activate NF-κB do so through a common pathway based on phosphorylation-induced, proteasome-mediated degradation of IκB (3-7). The key regulatory step in this pathway involves activation of a high molecular weight IκB kinase (IKK) complex whose catalysis is generally carried out by three tightly associated IKK subunits. IKKα and IKKβ serve as the catalytic subunits of the kinase and IKKγ serves as the regulatory subunit (8,9). Activation of IKK depends upon phosphorylation at Ser177 and Ser181 in the activation loop of IKKβ (Ser176 and Ser180 in IKKα), which causes conformational changes, resulting in kinase activation (10-13).

$260
100 µl
APPLICATIONS
REACTIVITY
Human, Monkey

Application Methods: Flow Cytometry, Immunofluorescence (Immunocytochemistry), Western Blotting

Background: The NF-κB/Rel transcription factors are present in the cytosol in an inactive state, complexed with the inhibitory IκB proteins (1-3). Most agents that activate NF-κB do so through a common pathway based on phosphorylation-induced, proteasome-mediated degradation of IκB (3-7). The key regulatory step in this pathway involves activation of a high molecular weight IκB kinase (IKK) complex whose catalysis is generally carried out by three tightly associated IKK subunits. IKKα and IKKβ serve as the catalytic subunits of the kinase and IKKγ serves as the regulatory subunit (8,9). Activation of IKK depends upon phosphorylation at Ser177 and Ser181 in the activation loop of IKKβ (Ser176 and Ser180 in IKKα), which causes conformational changes, resulting in kinase activation (10-13).

$260
100 µl
APPLICATIONS
REACTIVITY
Human, Mouse, Rat

Application Methods: Immunoprecipitation, Western Blotting

Background: The NF-κB/Rel transcription factors are present in the cytosol in an inactive state, complexed with the inhibitory IκB proteins (1-3). Most agents that activate NF-κB do so through a common pathway based on phosphorylation-induced, proteasome-mediated degradation of IκB (3-7). The key regulatory step in this pathway involves activation of a high molecular weight IκB kinase (IKK) complex whose catalysis is generally carried out by three tightly associated IKK subunits. IKKα and IKKβ serve as the catalytic subunits of the kinase and IKKγ serves as the regulatory subunit (8,9). Activation of IKK depends upon phosphorylation at Ser177 and Ser181 in the activation loop of IKKβ (Ser176 and Ser180 in IKKα), which causes conformational changes, resulting in kinase activation (10-13).

$260
100 µl
APPLICATIONS
REACTIVITY
Human, Monkey, Mouse, Rat

Application Methods: Western Blotting

Background: The NF-κB/Rel transcription factors are present in the cytosol in an inactive state, complexed with the inhibitory IκB proteins (1-3). Most agents that activate NF-κB do so through a common pathway based on phosphorylation-induced, proteasome-mediated degradation of IκB (3-7). The key regulatory step in this pathway involves activation of a high molecular weight IκB kinase (IKK) complex whose catalysis is generally carried out by three tightly associated IKK subunits. IKKα and IKKβ serve as the catalytic subunits of the kinase and IKKγ serves as the regulatory subunit (8,9). Activation of IKK depends upon phosphorylation at Ser177 and Ser181 in the activation loop of IKKβ (Ser176 and Ser180 in IKKα), which causes conformational changes, resulting in kinase activation (10-13).

$260
100 µl
APPLICATIONS
REACTIVITY
Human, Monkey, Mouse, Rat

Application Methods: Immunoprecipitation, Western Blotting

Background: The NF-κB/Rel transcription factors are present in the cytosol in an inactive state, complexed with the inhibitory IκB proteins (1-3). Most agents that activate NF-κB do so through a common pathway based on phosphorylation-induced, proteasome-mediated degradation of IκB (3-7). The key regulatory step in this pathway involves activation of a high molecular weight IκB kinase (IKK) complex whose catalysis is generally carried out by three tightly associated IKK subunits. IKKα and IKKβ serve as the catalytic subunits of the kinase and IKKγ serves as the regulatory subunit (8,9). Activation of IKK depends upon phosphorylation at Ser177 and Ser181 in the activation loop of IKKβ (Ser176 and Ser180 in IKKα), which causes conformational changes, resulting in kinase activation (10-13).

$111
20 µl
$260
100 µl
APPLICATIONS
REACTIVITY
Human, Rat

Application Methods: Western Blotting

Background: The NF-κB/Rel transcription factors are present in the cytosol in an inactive state, complexed with the inhibitory IκB proteins (1-3). Most agents that activate NF-κB do so through a common pathway based on phosphorylation-induced, proteasome-mediated degradation of IκB (3-7). The key regulatory step in this pathway involves activation of a high molecular weight IκB kinase (IKK) complex whose catalysis is generally carried out by three tightly associated IKK subunits. IKKα and IKKβ serve as the catalytic subunits of the kinase and IKKγ serves as the regulatory subunit (8,9). Activation of IKK depends upon phosphorylation at Ser177 and Ser181 in the activation loop of IKKβ (Ser176 and Ser180 in IKKα), which causes conformational changes, resulting in kinase activation (10-13).

$111
20 µl
$260
100 µl
APPLICATIONS
REACTIVITY
Human

Application Methods: Immunoprecipitation, Western Blotting

Background: The NF-κB/Rel transcription factors are present in the cytosol in an inactive state, complexed with the inhibitory IκB proteins (1-3). Most agents that activate NF-κB do so through a common pathway based on phosphorylation-induced, proteasome-mediated degradation of IκB (3-7). The key regulatory step in this pathway involves activation of a high molecular weight IκB kinase (IKK) complex whose catalysis is generally carried out by three tightly associated IKK subunits. IKKα and IKKβ serve as the catalytic subunits of the kinase and IKKγ serves as the regulatory subunit (8,9). Activation of IKK depends upon phosphorylation at Ser177 and Ser181 in the activation loop of IKKβ (Ser176 and Ser180 in IKKα), which causes conformational changes, resulting in kinase activation (10-13).

$348
50 tests
100 µl
This Cell Signaling Technology antibody is conjugated to phycoerythrin (PE) and tested in-house for direct flow cytometry analysis in mouse cells. This antibody is expected to exhibit the same species cross-reactivity as the unconjugated IKKε (D61F9) XP® Rabbit mAb #3416.
APPLICATIONS
REACTIVITY
Mouse, Rat

Application Methods: Flow Cytometry

Background: The NF-κB/Rel transcription factors are present in the cytosol in an inactive state, complexed with the inhibitory IκB proteins (1-3). Most agents that activate NF-κB do so through a common pathway based on phosphorylation-induced, proteasome-mediated degradation of IκB (3-7). The key regulatory step in this pathway involves activation of a high molecular weight IκB kinase (IKK) complex whose catalysis is generally carried out by three tightly associated IKK subunits. IKKα and IKKβ serve as the catalytic subunits of the kinase and IKKγ serves as the regulatory subunit (8,9). Activation of IKK depends upon phosphorylation at Ser177 and Ser181 in the activation loop of IKKβ (Ser176 and Ser180 in IKKα), which causes conformational changes, resulting in kinase activation (10-13).

$122
20 µl
$293
100 µl
APPLICATIONS
REACTIVITY
Mouse, Rat

Application Methods: Flow Cytometry, Immunofluorescence (Immunocytochemistry), Immunoprecipitation, Western Blotting

Background: The NF-κB/Rel transcription factors are present in the cytosol in an inactive state, complexed with the inhibitory IκB proteins (1-3). Most agents that activate NF-κB do so through a common pathway based on phosphorylation-induced, proteasome-mediated degradation of IκB (3-7). The key regulatory step in this pathway involves activation of a high molecular weight IκB kinase (IKK) complex whose catalysis is generally carried out by three tightly associated IKK subunits. IKKα and IKKβ serve as the catalytic subunits of the kinase and IKKγ serves as the regulatory subunit (8,9). Activation of IKK depends upon phosphorylation at Ser177 and Ser181 in the activation loop of IKKβ (Ser176 and Ser180 in IKKα), which causes conformational changes, resulting in kinase activation (10-13).

$293
100 µl
APPLICATIONS
REACTIVITY
Human

Application Methods: Flow Cytometry, Western Blotting

Background: Interleukin-10 (IL-10) is an anti-inflammatory cytokine that is produced by T cells, NK cells, and macrophages (1,2). IL-10 initiates signal transduction by binding to a cell surface receptor complex consisting of IL-10 RI and IL-10 RII (1), leading to the activation of Jak1 and Tyk2 and phosphorylation of Stat3 (1,3). The anti-inflammatory activity of IL-10 is due to its ability to block signaling through other cytokine receptors, notably IFN-γ receptor, by upregulating expression of SOCS1 (1,3). In addition, IL-10 promotes T cell tolerance by inhibiting tyrosine phosphorylation of CD28 (4,5). IL-10 is an important negative regulator of the immune response, which allows for maintenance of pregnancy (1). In contrast, increased IL-10 levels contribute to persistent Leishmania major infections (6).

$260
100 µl
APPLICATIONS
REACTIVITY
Human

Application Methods: Flow Cytometry, Immunohistochemistry (Paraffin), Immunoprecipitation, Western Blotting

Background: Cancer/testis antigens (CTAs) are a family of more than 100 proteins whose normal expression is largely restricted to immune privileged germ cells of the testis, ovary, and trophoblast cells of the placenta. Although most normal somatic tissues are void of CTA expression, due to epigenetic silencing of gene expression, their expression is upregulated in a wide variety of human solid and liquid tumors (1,2). As such, CTAs have garnered much attention as attractive targets for a variety of immunotherapy-based approaches to selectively attack tumors (3).

$305
50 tests
100 µl
This Cell Signaling Technology antibody is conjugated to phycoerythrin (PE) and tested in-house for direct flow cytometry analysis in mouse cells. This antibody is expected to exhibit the same species cross-reactivity as the unconjugated IL-17A (D1X7L) Rabbit mAb (Mouse Specific) #13838.
APPLICATIONS
REACTIVITY
Mouse

Application Methods: Flow Cytometry

Background: The IL-17 family of cytokines consists of IL-17A-F, and their receptors include IL-17RA-RE (1). IL-17 cytokines are produced by a variety of cell types including the Th17 subset of CD4+ T cells, as well as subsets of γδ T cells, NK cells, and NKT cells (2). IL-17A and IL-17F, the most well-studied of the IL-17 cytokines, contribute to fungal and bacterial immunity by inducing expression of proinflammatory cytokines, chemokines, and antimicrobial peptides (2). In addition, IL-17A contributes to the pathogenesis of several autoimmune diseases (3). IL-17E promotes Th2 cell responses (4). The roles of IL-17B, IL-17C, and IL-17D are less clear, however these family members also appear to have the capacity to induce proinflammatory cytokines (1,5,6). IL-17 receptors have an extracellular domain, a transmembrane domain, and a SEFIR domain. They are believed to signal as homodimers, heterodimers, or multimers through their SEFIR domain by recruiting the SEFIR domain-containing adaptor Act1 (7). Unlike most cytokines that signal through Jak/STAT pathways, IL-17 signaling results in NF-κB activation (8).

$260
100 µl
APPLICATIONS
REACTIVITY
Mouse

Application Methods: Flow Cytometry, Immunoprecipitation, Western Blotting

Background: The IL-17 family of cytokines consists of IL-17A-F, and their receptors include IL-17RA-RE (1). IL-17 cytokines are produced by a variety of cell types including the Th17 subset of CD4+ T cells, as well as subsets of γδ T cells, NK cells, and NKT cells (2). IL-17A and IL-17F, the most well-studied of the IL-17 cytokines, contribute to fungal and bacterial immunity by inducing expression of proinflammatory cytokines, chemokines, and antimicrobial peptides (2). In addition, IL-17A contributes to the pathogenesis of several autoimmune diseases (3). IL-17E promotes Th2 cell responses (4). The roles of IL-17B, IL-17C, and IL-17D are less clear, however these family members also appear to have the capacity to induce proinflammatory cytokines (1,5,6). IL-17 receptors have an extracellular domain, a transmembrane domain, and a SEFIR domain. They are believed to signal as homodimers, heterodimers, or multimers through their SEFIR domain by recruiting the SEFIR domain-containing adaptor Act1 (7). Unlike most cytokines that signal through Jak/STAT pathways, IL-17 signaling results in NF-κB activation (8).

$260
100 µl
APPLICATIONS
REACTIVITY
Mouse

Application Methods: Flow Cytometry, Western Blotting

Background: The IL-17 family of cytokines consists of IL-17A-F, and their receptors include IL-17RA-RE (1). IL-17 cytokines are produced by a variety of cell types including the Th17 subset of CD4+ T cells, as well as subsets of γδ T cells, NK cells, and NKT cells (2). IL-17A and IL-17F, the most well-studied of the IL-17 cytokines, contribute to fungal and bacterial immunity by inducing expression of proinflammatory cytokines, chemokines, and antimicrobial peptides (2). In addition, IL-17A contributes to the pathogenesis of several autoimmune diseases (3). IL-17E promotes Th2 cell responses (4). The roles of IL-17B, IL-17C, and IL-17D are less clear, however these family members also appear to have the capacity to induce proinflammatory cytokines (1,5,6). IL-17 receptors have an extracellular domain, a transmembrane domain, and a SEFIR domain. They are believed to signal as homodimers, heterodimers, or multimers through their SEFIR domain by recruiting the SEFIR domain-containing adaptor Act1 (7). Unlike most cytokines that signal through Jak/STAT pathways, IL-17 signaling results in NF-κB activation (8).

$260
100 µl
APPLICATIONS
REACTIVITY
Human

Application Methods: Western Blotting

Background: The IL-17 family of cytokines consists of IL-17A-F, and their receptors include IL-17RA-RE (1). IL-17 cytokines are produced by a variety of cell types including the Th17 subset of CD4+ T cells, as well as subsets of γδ T cells, NK cells, and NKT cells (2). IL-17A and IL-17F, the most well-studied of the IL-17 cytokines, contribute to fungal and bacterial immunity by inducing expression of proinflammatory cytokines, chemokines, and antimicrobial peptides (2). In addition, IL-17A contributes to the pathogenesis of several autoimmune diseases (3). IL-17E promotes Th2 cell responses (4). The roles of IL-17B, IL-17C, and IL-17D are less clear, however these family members also appear to have the capacity to induce proinflammatory cytokines (1,5,6). IL-17 receptors have an extracellular domain, a transmembrane domain, and a SEFIR domain. They are believed to signal as homodimers, heterodimers, or multimers through their SEFIR domain by recruiting the SEFIR domain-containing adaptor Act1 (7). Unlike most cytokines that signal through Jak/STAT pathways, IL-17 signaling results in NF-κB activation (8).

$260
100 µl
APPLICATIONS
REACTIVITY
Human

Application Methods: Western Blotting

Background: The founding members of the interleukin-1 (IL-1) superfamily include pro-inflammatory cytokines IL-1α and IL-1β, and a third protein that acts as an IL-1 receptor antagonist (IL-1RA). At least six similar proteins have been recently identified, including a homolog of IL-1RA (IL1F5). The three better-characterized proteins (IL-1a, IL-1b and IL-1RA) are mainly expressed in macrophages, monocytes, and dendritic cells. IL-1a and IL-1b act as potent inflammatory cytokines that help regulate host defense and immune responses (1). Binding of these pro-inflammatory cytokines to an IL-1 receptor recruits adapter proteins (such as IRAK) to the receptor. Phosphorylation of these adaptor proteins promotes downstream signaling cascades associated with the immune response (2). Altered expression of both IL-1a and IL-1b is associated with an extensive list of human disorders, including Alzheimer's disease, rheumatoid arthritis, psoriasis and various forms of cancer (3,4). IL-1RA acts as an anti-inflammatory cytokine, binding the IL-1 receptor to limit the response to inflammation (5). Because it plays a key role in regulating the inflammatory response, recombinant IL-1RA is a therapeutic agent used in the treatment of diseases such as rheumatoid arthritis. Alternatively, mutation of the corresponding IL-1RA gene may be associated with susceptibility to the development of specific cancers (6).