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Monoclonal Antibody interleukin-6 Receptor Binding

$260
100 µl
APPLICATIONS
REACTIVITY
Human

Application Methods: Immunoprecipitation, Western Blotting

Background: Acute phase response is induced by interleukin-6 (IL-6) produced by T cells, macrophages, fibroblasts, endothelial and other cells (1,2). IL-6 induces proliferation or differentiation in many cell types including B cells, thymocytes and T cells. IL-6, in concert with TGF-β, is important for developing Th17 responses. IL-6 binds to IL-6Rα and through this association induces gp130 homodimerization (1). gp130 homodimerization triggers the Jak/Stat cascade and the SHP-2/Erk MAP kinase cascade (1,3,4). IL-6 also forms a complex with an IL-6Rα splice variant that is nonmembrane-associated (3). The IL-6/soluble IL-6Rα complex can then activate the gp130 signaling pathway in cells that express gp130 but not IL-6Rα (3). Research studies have shown that IL-6, through increasing expression of proangiogenic VEGF, may also contribute to metastatic breast cancer (5).

$122
20 µl
$293
100 µl
APPLICATIONS
REACTIVITY
Mouse

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

Background: Acute phase response is induced by interleukin-6 (IL-6) produced by T cells, macrophages, fibroblasts, endothelial and other cells (1,2). IL-6 induces proliferation or differentiation in many cell types including B cells, thymocytes and T cells. IL-6, in concert with TGF-β, is important for developing Th17 responses. IL-6 binds to IL-6Rα and through this association induces gp130 homodimerization (1). gp130 homodimerization triggers the Jak/Stat cascade and the SHP-2/Erk MAP kinase cascade (1,3,4). IL-6 also forms a complex with an IL-6Rα splice variant that is nonmembrane-associated (3). The IL-6/soluble IL-6Rα complex can then activate the gp130 signaling pathway in cells that express gp130 but not IL-6Rα (3). Research studies have shown that IL-6, through increasing expression of proangiogenic VEGF, may also contribute to metastatic breast cancer (5).

$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. The antibody is expected to exhibit the same species cross-reactivity as the unconjugated IL-6 (D5W4V) XP® Rabbit mAb (Mouse Specific) #12912.
APPLICATIONS
REACTIVITY
Mouse

Application Methods: Flow Cytometry

Background: Acute phase response is induced by interleukin-6 (IL-6) produced by T cells, macrophages, fibroblasts, endothelial and other cells (1,2). IL-6 induces proliferation or differentiation in many cell types including B cells, thymocytes and T cells. IL-6, in concert with TGF-β, is important for developing Th17 responses. IL-6 binds to IL-6Rα and through this association induces gp130 homodimerization (1). gp130 homodimerization triggers the Jak/Stat cascade and the SHP-2/Erk MAP kinase cascade (1,3,4). IL-6 also forms a complex with an IL-6Rα splice variant that is nonmembrane-associated (3). The IL-6/soluble IL-6Rα complex can then activate the gp130 signaling pathway in cells that express gp130 but not IL-6Rα (3). Research studies have shown that IL-6, through increasing expression of proangiogenic VEGF, may also contribute to metastatic breast cancer (5).

$121
2 western blots
20 µl
$305
50 tests
100 µl
This Cell Signaling Technology antibody is conjugated to Alexa Fluor® 488 fluorescent dye and tested in-house for direct immunofluorescence analysis in mouse cells. This antibody is expected to exhibit the same species cross-reactivity as the unconjugated ASC (D2W8U) Rabbit mAb (Mouse Specific) #67824.
APPLICATIONS
REACTIVITY
Mouse

Application Methods: Flow Cytometry, Immunofluorescence (Immunocytochemistry)

Background: TMS1 (target of methylation-induced silencing)/ASC (apoptosis-associated speck-like protein containing a CARD), also referred to as PYCARD and CARD5, is a 22-kDa pro-apoptotic protein containing an N-terminal pyrin domain (PYD) and a C-terminal caspase recruitment domain (CARD) (1-2). The ASC/TMS1 gene was originally found to be aberrantly methylated and silenced in breast cancer cells (2), and has since been found to be silenced in a number of other cancers, including ovarian cancer (3), glioblastoma (4), melanoma (5), gastric cancer (6), lung cancer (7), and prostate cancer (8). Expression of ASC/TMS1 can be induced by pro-apoptotic/inflammatory stimuli (9). During apoptosis ASC/TMS1 is re-distributed from the cytosol to the mitochondria and associates with mitochondrial Bax to trigger cytochrome c release and subsequent apoptosis (10). ASC/TMS1 has also been found to be a critical component of inflammatory signaling where it associates with and activates caspase-1 in response to pro-inflammatory signals (11).

$305
50 tests
100 µl
This Cell Signaling Technology antibody is conjugated to phycoerythrin (PE) 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 ASC (D2W8U) Rabbit mAb (Mouse Specific) #67824.
APPLICATIONS
REACTIVITY
Mouse

Application Methods: Flow Cytometry

Background: TMS1 (target of methylation-induced silencing)/ASC (apoptosis-associated speck-like protein containing a CARD), also referred to as PYCARD and CARD5, is a 22-kDa pro-apoptotic protein containing an N-terminal pyrin domain (PYD) and a C-terminal caspase recruitment domain (CARD) (1-2). The ASC/TMS1 gene was originally found to be aberrantly methylated and silenced in breast cancer cells (2), and has since been found to be silenced in a number of other cancers, including ovarian cancer (3), glioblastoma (4), melanoma (5), gastric cancer (6), lung cancer (7), and prostate cancer (8). Expression of ASC/TMS1 can be induced by pro-apoptotic/inflammatory stimuli (9). During apoptosis ASC/TMS1 is re-distributed from the cytosol to the mitochondria and associates with mitochondrial Bax to trigger cytochrome c release and subsequent apoptosis (10). ASC/TMS1 has also been found to be a critical component of inflammatory signaling where it associates with and activates caspase-1 in response to pro-inflammatory signals (11).

$111
20 µl
$260
100 µl
APPLICATIONS
REACTIVITY
Mouse

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

Background: TMS1 (target of methylation-induced silencing)/ASC (apoptosis-associated speck-like protein containing a CARD), also referred to as PYCARD and CARD5, is a 22-kDa pro-apoptotic protein containing an N-terminal pyrin domain (PYD) and a C-terminal caspase recruitment domain (CARD) (1-2). The ASC/TMS1 gene was originally found to be aberrantly methylated and silenced in breast cancer cells (2), and has since been found to be silenced in a number of other cancers, including ovarian cancer (3), glioblastoma (4), melanoma (5), gastric cancer (6), lung cancer (7), and prostate cancer (8). Expression of ASC/TMS1 can be induced by pro-apoptotic/inflammatory stimuli (9). During apoptosis ASC/TMS1 is re-distributed from the cytosol to the mitochondria and associates with mitochondrial Bax to trigger cytochrome c release and subsequent apoptosis (10). ASC/TMS1 has also been found to be a critical component of inflammatory signaling where it associates with and activates caspase-1 in response to pro-inflammatory signals (11).

$305
50 tests
100 µl
This Cell Signaling Technology antibody is conjugated to Alexa Fluor® 647 fluorescent dye and tested in-house for direct immunofluorescent analysis in mouse cells. The antibody is expected to exhibit the same species cross-reactivity as the unconjugated ASC (D2W8U) Rabbit mAb (Mouse Specific) #67824.
APPLICATIONS
REACTIVITY
Mouse

Application Methods: Immunofluorescence (Immunocytochemistry)

Background: TMS1 (target of methylation-induced silencing)/ASC (apoptosis-associated speck-like protein containing a CARD), also referred to as PYCARD and CARD5, is a 22-kDa pro-apoptotic protein containing an N-terminal pyrin domain (PYD) and a C-terminal caspase recruitment domain (CARD) (1-2). The ASC/TMS1 gene was originally found to be aberrantly methylated and silenced in breast cancer cells (2), and has since been found to be silenced in a number of other cancers, including ovarian cancer (3), glioblastoma (4), melanoma (5), gastric cancer (6), lung cancer (7), and prostate cancer (8). Expression of ASC/TMS1 can be induced by pro-apoptotic/inflammatory stimuli (9). During apoptosis ASC/TMS1 is re-distributed from the cytosol to the mitochondria and associates with mitochondrial Bax to trigger cytochrome c release and subsequent apoptosis (10). ASC/TMS1 has also been found to be a critical component of inflammatory signaling where it associates with and activates caspase-1 in response to pro-inflammatory signals (11).

$260
100 µl
APPLICATIONS
REACTIVITY
Human

Application Methods: Immunoprecipitation, Western Blotting

Background: TMS1 (target of methylation-induced silencing)/ASC (apoptosis-associated speck-like protein containing a CARD), also referred to as PYCARD and CARD5, is a 22-kDa pro-apoptotic protein containing an N-terminal pyrin domain (PYD) and a C-terminal caspase recruitment domain (CARD) (1-2). The ASC/TMS1 gene was originally found to be aberrantly methylated and silenced in breast cancer cells (2), and has since been found to be silenced in a number of other cancers, including ovarian cancer (3), glioblastoma (4), melanoma (5), gastric cancer (6), lung cancer (7), and prostate cancer (8). Expression of ASC/TMS1 can be induced by pro-apoptotic/inflammatory stimuli (9). During apoptosis ASC/TMS1 is re-distributed from the cytosol to the mitochondria and associates with mitochondrial Bax to trigger cytochrome c release and subsequent apoptosis (10). ASC/TMS1 has also been found to be a critical component of inflammatory signaling where it associates with and activates caspase-1 in response to pro-inflammatory signals (11).

$111
20 µl
$260
100 µl
APPLICATIONS
REACTIVITY
Human

Application Methods: Western Blotting

Background: TACE (TNF-α converting enzyme), also known as ADAM17, is a transmembrane metalloprotease that plays a key role in the cleavage of a number cell surface molecules in a process known as “shedding". TACE is abundantly expressed in many adult tissues, but in fetal development expression is differentially regulated (1). An important substrate of TACE is pro-TNF-α (1). Increased expression of TACE is associated with several pathological conditions including osteoarthritis and rheumatoid arthritis, where the pro-inflammatory effects of increased TNF-α contribute to disease pathogenesis (2,3). Regulation of other important molecules by TACE such as EGFR and Notch has recently been documented. TACE is responsible for the shedding of EGFR ligands such as amphiregulin and TNF-α. Some tumors have hyperactivated EGFR due to upregulated TNF-α production and upregulated TACE, making TACE a potential target for drug development (4). TACE activates Notch in a ligand-independent manner and has been shown to play a role in the development of the Drosophila nervous system (5). TACE has also been proposed to act as α-secretase for amyloid precursor protein (APP) (6), and to be involved in the renewal and proliferation of neural stem cells (7).