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Mouse erbb-2 Class Receptor Binding

Also showing Human erbb-2 Class Receptor Binding

$260
100 µl
APPLICATIONS
REACTIVITY
Human, Mouse

Application Methods: Western Blotting

Background: Heregulin (HRG), also called neuregulin (NRG1), neu differentiation factor (NDF) or glial growth factor-2 (GGF-2), is a soluble growth factor synthesized as a transmembrane precursor molecule. Metalloproteinases and other proteases catalyze the cleavage of its extracellular domain which is then released and functions as a ligand for ErbB3 and ErbB4 receptor tyrosine kinase. The signaling pathways of HRG-ErbB3/ErbB4 are involved in regulation of cell proliferation, differentiation, invasion, and survival of both normal and malignant tissues (1,2). Abnormality of HRG-ErbB signaling leads to development of a variety of human diseases.HRG family has four isoforms including HRG-1, -2, -3 and -4, which are derived from alternative exon splicing. Moreover, they showed various tissue expression and biological activities (3).

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

Application Methods: Immunoprecipitation, Western Blotting

Background: Cyclin-dependent kinases (CDKs) are serine/threonine kinases that are activated by cyclins and govern eukaryotic cell cycle progression. While CDK5 shares high sequence homology with its family members, it is thought mainly to function in postmitotic neurons to regulate the cytoarchitecture of these cells. Analogous to cyclins, the regulatory subunits p35 and p39 associate with and activate CDK5 despite the lack of sequence homology. CDK5 is ubiquitously expressed, with high levels of kinase activity detected primarily in the nervous system due to the narrow expression pattern of p35 and p39 in post-mitotic neurons. A large number of CDK5 substrates have been identified although no substrates have been specifically attributed to p35 or p39. Substrates of CDK5 include p35, PAK1, Src, β-catenin, tau, neurofilament-H, neurofilament-M, synapsin-1, APP, DARPP32, PP1-inhibitor, and Rb. p35 is rapidly degraded (T1/2 <20 min) by the ubiquitin-proteasome pathway (1). However, p35 stability increases as CDK5 kinase activity decreases, likely as a result of decreased phosphorylation of p35 at Thr138 by CDK5 (2). Proteolytic cleavage of p35 by calpain produces p25 upon neurotoxic insult, resulting in prolonged activation of CDK5 by p25. Research studies have shown accumulation of p25 in neurodegenerative diseases, such as Alzheimer's disease and amyotrophic lateral sclerosis (ALS) (3,4).

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

Application Methods: Immunoprecipitation, Western Blotting

Background: Cyclin-dependent kinases (CDKs) are serine/threonine kinases that are activated by cyclins and govern eukaryotic cell cycle progression. While CDK5 shares high sequence homology with its family members, it is thought mainly to function in postmitotic neurons to regulate the cytoarchitecture of these cells. Analogous to cyclins, the regulatory subunits p35 and p39 associate with and activate CDK5 despite the lack of sequence homology. CDK5 is ubiquitously expressed, with high levels of kinase activity detected primarily in the nervous system due to the narrow expression pattern of p35 and p39 in post-mitotic neurons. A large number of CDK5 substrates have been identified although no substrates have been specifically attributed to p35 or p39. Substrates of CDK5 include p35, PAK1, Src, β-catenin, tau, neurofilament-H, neurofilament-M, synapsin-1, APP, DARPP32, PP1-inhibitor, and Rb. p35 is rapidly degraded (T1/2 <20 min) by the ubiquitin-proteasome pathway (1). However, p35 stability increases as CDK5 kinase activity decreases, likely as a result of decreased phosphorylation of p35 at Thr138 by CDK5 (2). Proteolytic cleavage of p35 by calpain produces p25 upon neurotoxic insult, resulting in prolonged activation of CDK5 by p25. Research studies have shown accumulation of p25 in neurodegenerative diseases, such as Alzheimer's disease and amyotrophic lateral sclerosis (ALS) (3,4).

$489
96 assays
1 Kit
The PathScan® Total CDK5 Sandwich ELISA Kit is a solid phase sandwich enzyme-linked immunosorbent assay (ELISA) that detects endogenous levels of CDK5 protein. A CDK5 mouse mAb has been coated onto the microwells. After incubation with cell lysates, the CDK5 protein is captured by the coated antibody. Following extensive washing, CDK5 rabbit detection mAb is added to detect captured CDK5 protein. Anti-rabbit, HRP-linked antibody is then used to recognize the bound detection antibody. HRP substrate, TMB, is added to develop color. The magnitude of absorbance for the developed color is proportional to the quantity of CDK5 protein.Antibodies in the kit are custom formulations specific to the kit.
REACTIVITY
Human, Monkey, Mouse, Rat

Background: Cyclin-dependent kinases (CDKs) are serine/threonine kinases that are activated by cyclins and govern eukaryotic cell cycle progression. While CDK5 shares high sequence homology with its family members, it is thought mainly to function in postmitotic neurons to regulate the cytoarchitecture of these cells. Analogous to cyclins, the regulatory subunits p35 and p39 associate with and activate CDK5 despite the lack of sequence homology. CDK5 is ubiquitously expressed, with high levels of kinase activity detected primarily in the nervous system due to the narrow expression pattern of p35 and p39 in post-mitotic neurons. A large number of CDK5 substrates have been identified although no substrates have been specifically attributed to p35 or p39. Substrates of CDK5 include p35, PAK1, Src, β-catenin, tau, neurofilament-H, neurofilament-M, synapsin-1, APP, DARPP32, PP1-inhibitor, and Rb. p35 is rapidly degraded (T1/2 <20 min) by the ubiquitin-proteasome pathway (1). However, p35 stability increases as CDK5 kinase activity decreases, likely as a result of decreased phosphorylation of p35 at Thr138 by CDK5 (2). Proteolytic cleavage of p35 by calpain produces p25 upon neurotoxic insult, resulting in prolonged activation of CDK5 by p25. Research studies have shown accumulation of p25 in neurodegenerative diseases, such as Alzheimer's disease and amyotrophic lateral sclerosis (ALS) (3,4).

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

Application Methods: Immunoprecipitation, Western Blotting

Background: Cyclin-dependent kinases (CDKs) are serine/threonine kinases that are activated by cyclins and govern eukaryotic cell cycle progression. While CDK5 shares high sequence homology with its family members, it is thought mainly to function in postmitotic neurons to regulate the cytoarchitecture of these cells. Analogous to cyclins, the regulatory subunits p35 and p39 associate with and activate CDK5 despite the lack of sequence homology. CDK5 is ubiquitously expressed, with high levels of kinase activity detected primarily in the nervous system due to the narrow expression pattern of p35 and p39 in post-mitotic neurons. A large number of CDK5 substrates have been identified although no substrates have been specifically attributed to p35 or p39. Substrates of CDK5 include p35, PAK1, Src, β-catenin, tau, neurofilament-H, neurofilament-M, synapsin-1, APP, DARPP32, PP1-inhibitor, and Rb. p35 is rapidly degraded (T1/2 <20 min) by the ubiquitin-proteasome pathway (1). However, p35 stability increases as CDK5 kinase activity decreases, likely as a result of decreased phosphorylation of p35 at Thr138 by CDK5 (2). Proteolytic cleavage of p35 by calpain produces p25 upon neurotoxic insult, resulting in prolonged activation of CDK5 by p25. Research studies have shown accumulation of p25 in neurodegenerative diseases, such as Alzheimer's disease and amyotrophic lateral sclerosis (ALS) (3,4).