CaMKI Antibody [G24K20]

Catalog No.: F2963

Application: Reactivity: Mouse, Rat, Human

Lane 1: 293T, Lane 2: NIH/3T3, Lane 3: PC-12, Lane 4: Mouse brain

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代表番号: 045-509-1970|電子メール：sales@selleck.co.jp

使用情報

Dilution
WB1:5000 - 1:10000 IHC1:100 - 1:250

Application
WB, IHC

Source
Rabbit Monoclonal Antibody

Reactivity
Mouse, Rat, Human

Storage Buffer
PBS, pH 7.2+50% Glycerol+0.05% BSA+0.01% NaN3

Storage (from the date of receipt)
-20°C (avoid freeze-thaw cycles), 2 years

Predicted MW Observed MW
41 kDa 41 kDa
^*なぜ予測分子量と実際の分子量が異なるのか？下記の原因により、実際の分子量が予測と異なる：タンパク質の翻訳後修飾（リン酸化/糖鎖付加），スプライシングバリアント，イソフォーム，相対的な電荷，ポリマー。

Datasheet & SDS

生物学的記述

Specificity
CaMKI Antibody [G24K20] detects endogenous levels of total CaMKI protein.

Clone
G24K20

Synonym(s)
Calcium/calmodulin-dependent protein kinase type 1; CaM kinase I; CaM kinase I alpha; CaM-KI; CaMKI-alpha; CAMK1

Background
CaMKI (Calcium/Calmodulin-dependent protein kinase I, CAMK1) is a serine/threonine kinase of the CaMK family encoded by CAMK1 on chromosome 3, existing as 370-amino acid isoforms (~42 kDa) ubiquitously expressed in brain, muscle, liver, and other tissues. CaMKI features an N-terminal catalytic kinase domain (residues 1-294) with ATP-binding glycine-rich loop and substrate cleft, followed by a multifunctional regulatory domain (295-370) containing autoinhibitory helix-loop-helix (Ile286-Met316) that blocks the active site, calmodulin-binding segment (post-306), and Thr177 phosphorylation site for full activation. Activation occurs via Ca²⁺/CaM binding displacing autoinhibition (K_{0.5} ~30 nM CaM), enabling basal phosphorylation by CaMKK at Thr177; subsequent autophosphorylation or Thr177 modification sustains activity post-CaM dissociation. CaMKI phosphorylates synapsin I, CREB, and transcription factors to regulate synaptic plasticity, neurotransmitter release, neuronal gene expression, axon growth, aldosterone synthesis, cell cycle progression, and long-term potentiation critical for learning/memory. Dysregulated CaMKI contributes to neurodegeneration (cognitive impairment via synapsin I defects), cardiac hypertrophy, and altered neuronal excitability in epilepsy models.

Background

CaMKI (Calcium/Calmodulin-dependent protein kinase I, CAMK1) is a serine/threonine kinase of the CaMK family encoded by CAMK1 on chromosome 3, existing as 370-amino acid isoforms (~42 kDa) ubiquitously expressed in brain, muscle, liver, and other tissues. CaMKI features an N-terminal catalytic kinase domain (residues 1-294) with ATP-binding glycine-rich loop and substrate cleft, followed by a multifunctional regulatory domain (295-370) containing autoinhibitory helix-loop-helix (Ile286-Met316) that blocks the active site, calmodulin-binding segment (post-306), and Thr177 phosphorylation site for full activation. Activation occurs via Ca²⁺/CaM binding displacing autoinhibition (K_{0.5} ~30 nM CaM), enabling basal phosphorylation by CaMKK at Thr177; subsequent autophosphorylation or Thr177 modification sustains activity post-CaM dissociation. CaMKI phosphorylates synapsin I, CREB, and transcription factors to regulate synaptic plasticity, neurotransmitter release, neuronal gene expression, axon growth, aldosterone synthesis, cell cycle progression, and long-term potentiation critical for learning/memory. Dysregulated CaMKI contributes to neurodegeneration (cognitive impairment via synapsin I defects), cardiac hypertrophy, and altered neuronal excitability in epilepsy models.

References
[1] Picciotto MR, et al. Adv Pharmacol. 1996;36:251-75. [2] Junho CVC, et al. Front Physiol. 2020 Jul 14;11:735.

PVDFメンブレン孔径参考表

Protein Size (kDa)	PVDF Transfer Membrane Pore Size (μm)
< 10	0.22
10-20	0.22
20-30	0.45
30-45	0.45
45-70	0.45
80-100	0.45
100-140	0.45
> 140	0.45

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Protein Size (kDa)	Separating Gel Percentage
4-40	20%
12-45	15%
10-70	12.5%
15-100	10%
25-100	8%
60-210	5%