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  2. Monoclonal

SMC-305

HCN2 Antibody, Clone S71

Cannot supply to this region.

SKU:
SMC-305
Additional Names:
BCNG2, HAC1, brain cyclic nucleotide gated channel 2, Potassium/sodium hyperpolarization-activated cyclic nucleotide-gated channel
Application:
IHC, WB, IF, ICC, IP, Microarray
Concentration:
1 mg/ml
Species Reactivity:
Rat
Purification:
Protein G Purified
Storage Conditions:
-20[o]C
Supplier:
StressMarq Biosciences
Host:
Mouse
Reactivities:
Mouse, Rat
ABP:
IMP-GEN-2015-06 < 10% Serum <100ml
Buffer:
PBS pH7.4, 50% glycerol, 0.09% sodium azide
Immunogen:
Fusion protein amino acids 761-863 (cytoplasmic C-terminus) of rat HCN2
Clone:
S71
Uniprot:
Q9JKA9
Synonyms:
hyperpolarization activated cyclic nucleotide-gated potassium channel 2;potassium/sodium hyperpolarization-activated cyclic nucleotide-gated channel 2
Extra Details:
HCN2 is a member of the hyperpolarization-activated cyclic nucleotide-gated (HCN) channel family, widely expressed in both the central and peripheral nervous systems. It contributes to the generation of pacemaker currents (I_h) that regulate neuronal excitability, rhythmic firing, and synaptic transmission. In the brain, HCN2 is particularly important for maintaining the excitability of thalamocortical and hippocampal neurons. Dysregulation of HCN2 has been implicated in several neurological and neurodegenerative disorders, including epilepsy, chronic pain, and Parkinson's disease. HCN2 dysfunction can lead to abnormal neuronal firing patterns, increased susceptibility to seizures, and impaired sensory processing. In neurodegenerative contexts, altered HCN2 expression may exacerbate network instability and contribute to cognitive and motor deficits. Additionally, HCN2 channels are modulated by cyclic nucleotides such as cAMP, linking them to intracellular signaling pathways that are often disrupted in neurodegeneration. Their role in regulating neuronal excitability and plasticity makes HCN2 a promising candidate for therapeutic modulation in diseases characterized by circuit dysfunction and progressive neuronal loss.
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