DUSP4 Antibody [F2A21] | Primary Antibodies

Application: Reactivity: Human, Monkey

Usage Information

Dilution
WB1:1000

Application
WB

Reactivity
Human, Monkey

Source
Rabbit Monoclonal Antibody

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
42 kDa

Datasheet & SDS

Biological Description

Specificity
DUSP4 Antibody [F2A21] detects endogenous levels of total DUSP4 protein.

Clone
F2A21

Synonym(s)
Dual specificity protein phosphatase 4; Dual specificity protein phosphatase hVH2; Mitogen-activated protein kinase phosphatase 2 (MAP kinase phosphatase 2; MKP-2); DUSP4; MKP2; VH2

Background
DUSP4 (dual specificity phosphatase 4, also known as MKP-2/hVH2) is a nuclear MAPK phosphatase that acts as a rapid, inducible negative feedback regulator of MAPK signaling, chiefly targeting ERK1/2 and JNK by dephosphorylating both phosphothreonine and phosphotyrosine residues. It features an N-terminal rhodanese-fold MAPK-docking domain and a C-terminal catalytic domain with the HCX5R motif, enabling dual substrate specificity. DUSP4 is swiftly upregulated in response to growth factors or Ras/Raf activation via ERK-, STAT3-, and p53-dependent transcription, leading to nuclear accumulation and termination of MAPK signaling (notably dephosphorylating p-ERK1/2 T202/Y204 and p-JNK T183/Y185), thereby restraining cell proliferation, differentiation, and inflammation while promoting senescence and apoptosis. It fine-tunes ERK/JNK/p38 pathways in immunity, development, stress responses, and metabolism, and is inactivated by ROS-mediated redox sensitivity. Dysregulation of DUSP4, loss in certain cancers (e.g., breast, colon) or overexpression in other contexts, can drive tumor progression or confer cytoprotection, respectively.

Background

DUSP4 (dual specificity phosphatase 4, also known as MKP-2/hVH2) is a nuclear MAPK phosphatase that acts as a rapid, inducible negative feedback regulator of MAPK signaling, chiefly targeting ERK1/2 and JNK by dephosphorylating both phosphothreonine and phosphotyrosine residues. It features an N-terminal rhodanese-fold MAPK-docking domain and a C-terminal catalytic domain with the HCX5R motif, enabling dual substrate specificity. DUSP4 is swiftly upregulated in response to growth factors or Ras/Raf activation via ERK-, STAT3-, and p53-dependent transcription, leading to nuclear accumulation and termination of MAPK signaling (notably dephosphorylating p-ERK1/2 T202/Y204 and p-JNK T183/Y185), thereby restraining cell proliferation, differentiation, and inflammation while promoting senescence and apoptosis. It fine-tunes ERK/JNK/p38 pathways in immunity, development, stress responses, and metabolism, and is inactivated by ROS-mediated redox sensitivity. Dysregulation of DUSP4, loss in certain cancers (e.g., breast, colon) or overexpression in other contexts, can drive tumor progression or confer cytoprotection, respectively.

References
https://pubmed.ncbi.nlm.nih.gov/25834604/ https://pubmed.ncbi.nlm.nih.gov/22812510/

Reference Table for Selecting PVDF Membrane Pore Size Specifications

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%