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ELK Biotechnology
SKU:ES3110
p35 rabbit pAb
p35 rabbit pAb
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$250.00 USD
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Applications: WB;IHC;IF;ELISA
Reactivity: Human;Mouse;Rat
Source: Rabbit
Dilution: Western Blot: 1/500 - 1/2000. Immunohistochemistry: 1/100 - 1/300. Immunofluorescence: 1/200 - 1/1000. ELISA: 1/20000. Not yet tested in other applications.
Immunogen: The antiserum was produced against synthesized peptide derived from human CDK5R1. AA range:11-60
Storage_stability: -20°C/1 year
Clonality: Polyclonal
Isotype: IgG
Concentration: 1 mg/ml
Observed_band(KD): 38kD
Human_gene_id: 8851
Human_swiss_prot_no: Q15078
Subcellular_location: [Cyclin-dependent kinase 5 activator 1, p35]: Cell membrane ; Lipid-anchor ; Cytoplasmic side . Cell projection, neuron projection . In the primary cortical neurons, p35 is present in the peripheries and nerve terminals. .; [Cyclin-dependent kinase 5 activator 1, p25]: Nucleus . Cytoplasm, perinuclear region . Perikaryon . The conversion of p35 to p25 relocalizes the protein from the cell periphery to the cytoplasm, in nuclear and perinuclear regions (PubMed:18507738). In the primary cortical neurons, p25 is primarily concentrated in the cell soma and is largely absent from neurites (PubMed:18507738). .
Other_name: CDK5R1; CDK5R; NCK5A; Cyclin-dependent kinase 5 activator 1; CDK5 activator 1; Cyclin-dependent kinase 5 regulatory subunit 1; TPKII regulatory subunit
Background: The protein encoded by this gene (p35) is a neuron-specific activator of cyclin-dependent kinase 5 (CDK5); the activation of CDK5 is required for proper development of the central nervous system. The p35 form of this protein is proteolytically cleaved by calpain, generating a p25 form. The cleavage of p35 into p25 results in relocalization of the protein from the cell periphery to nuclear and perinuclear regions. P25 deregulates CDK5 activity by prolonging its activation and changing its cellular location. The p25 form accumulates in the brain neurons of patients with Alzheimer's disease. This accumulation correlates with an increase in CDK5 kinase activity, and may lead to aberrantly phosphorylated forms of the microtubule-associated protein tau, which contributes to Alzheimer's disease. [provided by RefSeq, Jul 2008],
Reactivity: Human;Mouse;Rat
Source: Rabbit
Dilution: Western Blot: 1/500 - 1/2000. Immunohistochemistry: 1/100 - 1/300. Immunofluorescence: 1/200 - 1/1000. ELISA: 1/20000. Not yet tested in other applications.
Immunogen: The antiserum was produced against synthesized peptide derived from human CDK5R1. AA range:11-60
Storage_stability: -20°C/1 year
Clonality: Polyclonal
Isotype: IgG
Concentration: 1 mg/ml
Observed_band(KD): 38kD
Human_gene_id: 8851
Human_swiss_prot_no: Q15078
Subcellular_location: [Cyclin-dependent kinase 5 activator 1, p35]: Cell membrane ; Lipid-anchor ; Cytoplasmic side . Cell projection, neuron projection . In the primary cortical neurons, p35 is present in the peripheries and nerve terminals. .; [Cyclin-dependent kinase 5 activator 1, p25]: Nucleus . Cytoplasm, perinuclear region . Perikaryon . The conversion of p35 to p25 relocalizes the protein from the cell periphery to the cytoplasm, in nuclear and perinuclear regions (PubMed:18507738). In the primary cortical neurons, p25 is primarily concentrated in the cell soma and is largely absent from neurites (PubMed:18507738). .
Other_name: CDK5R1; CDK5R; NCK5A; Cyclin-dependent kinase 5 activator 1; CDK5 activator 1; Cyclin-dependent kinase 5 regulatory subunit 1; TPKII regulatory subunit
Background: The protein encoded by this gene (p35) is a neuron-specific activator of cyclin-dependent kinase 5 (CDK5); the activation of CDK5 is required for proper development of the central nervous system. The p35 form of this protein is proteolytically cleaved by calpain, generating a p25 form. The cleavage of p35 into p25 results in relocalization of the protein from the cell periphery to nuclear and perinuclear regions. P25 deregulates CDK5 activity by prolonging its activation and changing its cellular location. The p25 form accumulates in the brain neurons of patients with Alzheimer's disease. This accumulation correlates with an increase in CDK5 kinase activity, and may lead to aberrantly phosphorylated forms of the microtubule-associated protein tau, which contributes to Alzheimer's disease. [provided by RefSeq, Jul 2008],
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