RSK1 p90 Antibody [K1J12]

Catalog No.: F1108

Application: Reactivity: Mouse, Rat, Human

Lane 1: MCF7, Lane 2: K562, Lane 3: PC-12, Lane 4: Mouse lung

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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
WB1:1000 IP1:70 IHC1:100 IF1:150-1:200 FCM1:100-1:1000

Application
WB, IP, IHC, IF, FCM

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
83 kDa, 82 kDa 83 kDa,37 kDa, 90 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
RSK1 p90 Antibody [K1J12] detects endogenous levels of total RSK1 p90 protein.

Clone
K1J12

Synonym(s)
MAPKAPK1A; RSK1; RPS6KA1; Ribosomal protein S6 kinase alpha‑1; S6K‑alpha‑1; 90 kDa ribosomal protein S6 kinase 1; p90‑RSK 1; p90RSK1; p90S6K; MAPK‑activated protein kinase 1a; MAPKAP kinase 1a; MAPKAPK‑1a; RSK‑1

Background
RSK1 (p90 ribosomal S6 kinase 1), a serine/threonine kinase of the RSK family positioned at the terminus of the Ras/Raf/MEK/ERK cascade, receives extracellular growth factor signals to drive proliferation, survival, and motility across diverse tissues, including brain, muscle, and epithelia. ERK1/2 docks at its C-terminal kinase domain to initiate sequential phosphorylation culminating in PDK1-mediated activation of the N-terminal catalytic site, enabling RSK1 to phosphorylate over 30 substrates spanning transcription factors, cytoskeletal regulators, and feedback inhibitors. Activated RSK1 docks at the nucleus to phosphorylate CREB at Ser133, inducing immediate early genes like c-Fos and Bcl-2 that promote G1/S transition and apoptosis resistance, while cytoplasmic RSK1 inhibits TSC2 to activate mTORC1/S6K1 for protein synthesis and phosphorylates Mkl1 to enhance SRF transcription of actin cytoskeletal genes driving lamellipodia formation. This dual nuclear-cytoplasmic action integrates immediate mitogenic responses with long-term adaptive gene programs, as RSK1 phosphorylates p27kip1 for cytoplasmic retention to unleash cyclin E-CDK2 while feedback phosphorylating Raf-1 at Ser259 to dampen upstream ERK flux. RSK1 sustains synaptic plasticity through CREB-dependent transcription in hippocampal neurons and coordinates muscle hypertrophy via mTORC1 during exercise, making it a precise readout for researchers dissecting ERK pathway fidelity in neuronal cultures or tumor organoids via phospho-S380 antibodies. Constitutive activation via upstream RAS/RAF mutations fuels prostate cancer progression by enhancing AR transcriptional activity through p300/CBP coactivator synergy and chemoresistance via YB-1 stabilization.

Background

RSK1 (p90 ribosomal S6 kinase 1), a serine/threonine kinase of the RSK family positioned at the terminus of the Ras/Raf/MEK/ERK cascade, receives extracellular growth factor signals to drive proliferation, survival, and motility across diverse tissues, including brain, muscle, and epithelia. ERK1/2 docks at its C-terminal kinase domain to initiate sequential phosphorylation culminating in PDK1-mediated activation of the N-terminal catalytic site, enabling RSK1 to phosphorylate over 30 substrates spanning transcription factors, cytoskeletal regulators, and feedback inhibitors. Activated RSK1 docks at the nucleus to phosphorylate CREB at Ser133, inducing immediate early genes like c-Fos and Bcl-2 that promote G1/S transition and apoptosis resistance, while cytoplasmic RSK1 inhibits TSC2 to activate mTORC1/S6K1 for protein synthesis and phosphorylates Mkl1 to enhance SRF transcription of actin cytoskeletal genes driving lamellipodia formation. This dual nuclear-cytoplasmic action integrates immediate mitogenic responses with long-term adaptive gene programs, as RSK1 phosphorylates p27kip1 for cytoplasmic retention to unleash cyclin E-CDK2 while feedback phosphorylating Raf-1 at Ser259 to dampen upstream ERK flux. RSK1 sustains synaptic plasticity through CREB-dependent transcription in hippocampal neurons and coordinates muscle hypertrophy via mTORC1 during exercise, making it a precise readout for researchers dissecting ERK pathway fidelity in neuronal cultures or tumor organoids via phospho-S380 antibodies. Constitutive activation via upstream RAS/RAF mutations fuels prostate cancer progression by enhancing AR transcriptional activity through p300/CBP coactivator synergy and chemoresistance via YB-1 stabilization.

References
[1] Manhas N, et al. J Neurochem. 2010 Sep 1;114(5):1476-86. [2] Cronin R, et al. Oncogene. 2021 Jun;40(22):3775-3785.

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%