Purified anti-ERK1/2 Phospho (Thr202/Tyr204) Antibody, ERK1/2 Phospho, Poly21A07,BioLegend,604951

This clone was tested by ICC in HeLa cells treated with or without 100 ng/mL PMA. Three fix/perm methods were used: methanol fixation or 4% PFA fixation followed by permeabilization with either methanol or Triton X-100. All three methods resulted in weak staining and a lack of phospho-specificity.

Host

Rabbit

Reactivity

Human, Mouse

Application

WB - Quality tested

Platform ID

BAB311362412

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Product Specifications
Scientific Background

Specifications

NamePurified anti-ERK1/2 Phospho (Thr202/Tyr204) Antibody, ERK1/2 Phospho, Poly21A07
Cat. No.604951
HostRabbit
RRIDAB_2927813 (BioLegend Cat. No. 604951)AB_2927813 (BioLegend Cat. No. 604952)
IsotypeRabbit Polyclonal IgG
ReactivityHuman, Mouse
ApplicationWB - Quality tested
ClonalityPolyclonal
Clone NumberPoly21A07
ConcentrationLot-specific (to obtain lot-specific concentration and expiration, please enter the lot number in ourCertificate of Analysisonline tool.)
TargetERK1/2
ImmunogenSynthetic peptide of human Erk1/2 phosphorylated at Thr202/Tyr204
PurityThe antibody was purified by affinity chromatography.
FormulationPhosphate-buffered solution, pH 7.2, containing 0.09% sodium azide
StorageThe antibody solution should be stored undiluted between 2°C and 8°C.
Regulatory StatusResearch Use Only

Scientific Background

ERK1/2 (extracellular signal-regulated protein kinase) are members of the mitogen-activated protein kinase (MAPK) family of serine/threonine kinases. ERK1, also called Mitogen-activated protein kinase 3 (MAPK3) and ERK2, also called Mitogen-activated protein kinase 1 (MAPK1), are both integral effectors of the Ras-dependent extracellular signal-regulated kinase 1 (ERK1/2) mitogen-activated (MAP) kinase pathway. As such, they are vital regulators of cell cycle, differentiation, proliferation, stress-response, survival, and senescence. ERK1/2 are activated via phosphorylation of their tyrosine (Tyr204) and threonine (Thr202) residues by MEK1 and MEK2 in response to mitogenic stimuli. Upon activation, ERK1/2 translocate to the nucleus where they function in the regulation of transcription and translation. Dysregulation of ERK1/2 and the hyper-activation of the ERK pathway are characteristics of many cancers where it contributes to tumorigenesis, metastasis, and treatment-resistance, making ERK1/2 an important therapeutic target.

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