CaMKIV Antibody (YA5113)
(Synonyms: CAMK4; CAMK; CAMK-GR; CAMKIV; Calcium/calmodulin-dependent protein kinase type IV; CaMK IV; CaM kinase-GR)CaMKIV Antibody (YA5113) is a Mouse-derived and non-conjugated monoclonal antibody, targeting to CaMKIV.
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Host:
Mouse
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Application:
WB
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Reactivity :
Human, Mouse, Rat, Chicken, Dog, Pig
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Formulation:
Supplied in PBS containing 50% glycerol, 0.5% BSA and 0.02% sodium azide.
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Conjugation:
Non-conjugated
Applications
| Application |
WB
WB: Western Blot
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|---|---|
| Dilution Ratio | 1:1000-1:2000 |
Product Details
CaMKIV Antibody (YA5113) is a Mouse-derived and non-conjugated monoclonal antibody, targeting to CaMKIV.
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Host Mouse
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Clonality Monoclonal
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Species ReactivityHuman, Mouse, Rat, Chicken, Dog, Pig
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Calculated Molecular Weight Predicted band size: 52 kDa;
Purified recombinant human CaMKIV protein fragments expressed in E.coli.
affinity purified.
Non-conjugated
Unmodified
Product Properties
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Appearance
Solution
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Formulation
Supplied in PBS containing 50% glycerol, 0.5% BSA and 0.02% sodium azide.
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Storage & Stability
Stored at -20°C for 1 year. Avoid repeated freeze / thaw cycles.
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Shipping
Shipping with blue ice.
Background
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Function
CaMKIV (calcium/calmodulin-dependent protein kinase IV) is a calcium-responsive serine/threonine kinase that functions primarily in the nucleus to couple intracellular calcium signals with CRE-dependent transcription programs through phosphorylation of CREB.[1] Mechanistically, CaMKIV operates within the CaMKK-CaMKIV-CREB signaling axis, where upstream CaMKK activation promotes CREB phosphorylation and transcriptional responses associated with neuronal plasticity and activity-dependent gene expression.[2][3] Through this pathway, CaMKIV contributes to the regulation of c-Fos expression, late-phase long-term potentiation (L-LTP), and transcriptional processes required for long-term memory consolidation.[1] In disease-relevant and experimental models, disruption of CaMKIV signaling reduces activity-induced CREB phosphorylation and impairs hippocampus-dependent memory retention without markedly affecting basal synaptic transmission or early LTP, supporting its role in long-term neuronal adaptation.[1] Compared with the closely related CaMKII family, which participates broadly in synaptic signaling, CaMKIV shows a stronger association with nuclear transcriptional regulation and trophic CREB-dependent gene expression.[3] This distinction makes CaMKIV a useful experimental target for investigating calcium-dependent transcription, memory-associated signaling networks, and neuroprotective gene programs.[1][3] For research applications, pharmacological or genetic manipulation of the upstream CaMKK-CaMKIV pathway is commonly used to examine CREB-mediated transcriptional responses and neuronal plasticity mechanisms.[2][3]
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Subcellular Localization
Cytoplasm; Nucleus
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Expression
Tissue_specificity:It is expressed in brain, thymus, CD4 T cells, testes, and epithelial ovarian cancer tissues. -
Subunit
Monomer (By similarity). Interacts with protein phosphatase 2A (PPP2CA/PPP2CB); the interaction is mutually exclusive with binding to Ca(2+)/calmodulin
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SwissProt ID
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Synonyms
CAMK4; CAMK; CAMK-GR; CAMKIV; Calcium/calmodulin-dependent protein kinase type IV; CaMK IV; CaM kinase-GR
Documentation
References
[1]. Kang H, et al. An important role of neural activity-dependent CaMKIV signaling in the consolidation of long-term memory. Cell. 2001 Sep 21;106(6):771-83. [Content Brief]
[2]. Peters M, et al. Loss of Ca2+/calmodulin kinase kinase beta affects the formation of some, but not all, types of hippocampus-dependent long-term memory. J Neurosci. 2003 Oct 29;23(30):9752-60. [Content Brief]
[3]. Bell KF, et al. Calmodulin kinase IV-dependent CREB activation is required for neuroprotection via NMDA receptor-PSD95 disruption. J Neurochem. 2013 Jul;126(2):274-87. [Content Brief]