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anti-Human DUSP4 Antikörper:
anti-Mouse (Murine) DUSP4 Antikörper:
anti-Rat (Rattus) DUSP4 Antikörper:
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Frog Monoclonal DUSP4 Primary Antibody für IF, IP - ABIN968214
Black, Walker, Clark, MacLaren, Gillespie: Cell transformation by v-Jun deactivates ERK MAP kinase signalling. in Oncogene 2002
Show all 3 Pubmed References
Human Polyclonal DUSP4 Primary Antibody für IHC (p), IHC - ABIN446872
Manzano, Martinez-Navarro, Forteza, Brugarolas: Microarray phosphatome profiling of breast cancer patients unveils a complex phosphatase regulatory role of the MAPK and PI3K pathways in estrogen receptor-negative breast cancers. in International journal of oncology 2014
Human Monoclonal DUSP4 Primary Antibody für ELISA, WB - ABIN560663
Lee, Huang, Lee, Lee, Ryu, Kim, Kim, Kim, Joung, Kim, Shong, Jo: Dual specificity phosphatase 6 as a predictor of invasiveness in papillary thyroid cancer. in European journal of endocrinology / European Federation of Endocrine Societies 2012
our results indicate that Nodal regulated dusp4 plays a repressive role in mesendoderm induction.
dusp4 is essential for early development; knockout of dusp4 revealed a specific loss of sox17 (zeige SOX17 Antikörper), establishing a new class of endoderm specification defect.
Study revealed that DUSP4 expression was apparently downregulated in the deep region of colorectal cancer (CRC (zeige CALR Antikörper)) tissues compared with the superficial region, and that ERK (zeige EPHB2 Antikörper) phosphorylation was conversely increased in the deep region relative to the superficial region. Also, downregulation of DUSP4 in CRC (zeige CALR Antikörper) might promote cell proliferation and invasiveness through activation of ERK (zeige EPHB2 Antikörper).
Results show that DUSP4 gene is under-expressed in ER-negative breast cancer and is deleted in approximately 50 % of breast cancers. Induced DUSP4 expression suppresses both in vitro and in vivo growths of breast cancer cells suggesting that DUSP4 is a critical regulator of the growth and invasion of triple-negative breast cancer cells.
Our findings demonstrate a genetic mechanism by which pancreatic precursor lesions progress to invasive carcinomas and highlight DUSP4 as a novel invasion suppressor
DUSP4 is crucial in regulating corticosteroid sensitivity.
Data indicate that normalization of dual-specific phosphatase 4 (DUSP4) expression using a specific siRNA improved CD4(+) T-cell activity in idiopathic CD4 lymphopenia (ICL).
Ectopic expression of wild-type DUSP4, but not of a phosphatase-deficient mutant, dephosphorylates c-JUN N-terminal kinase (JNK) and induces apoptosis in DLBCL cells.
Low DUSP4 expression levels predict recurrence and mortality in triple-negative breast cancer patients
Data suggest that MKP-2 rather than MKP-1 is tamoxifen-regulated and that the elevated expression of MKP-2 in MCF7-TAMR cells potentially functions to restore tamoxifen sensitivity.
MKP-1 (zeige DUSP1 Antikörper) and MKP-2 stability is regulated by ERK (zeige EPHB2 Antikörper)-mediated phosphorylation through a degradation pathway independent of polyubiquitination
Instead, autophagic cell death was the major consequence, and our investigation of mechanisms suggested it is mediated via the dual specificity phosphatase-4 (DUSP4) dependent ERK (zeige EPHB2 Antikörper) inactivation pathway
domain-mapping results showed that both the substrate-interacting and the phosphatase domains of DUSP4 (zeige DUSP9 Antikörper) were required for its optimal interaction with STAT5 (zeige STAT5A Antikörper), while the coiled-coil domain of STAT5 (zeige STAT5A Antikörper) appeared to hinder this interaction
MKP-2 knock-out mice show deficits in working memory and spatial reference.
DUSP4 (zeige DUSP9 Antikörper) is crucial for neuronal differentiation and functions in the neurogenesis of embryonic stem cells.
Loss of MKP-2 expression is associated with enhanced susceptibility to parasite infection.
LH/hCG (zeige CGA Antikörper) tightly regulates MKP-2 expression, which modulates the induction of CYP11A1 (zeige CYP11A1 Antikörper) by 8Br-cAMP.
Dusp1 (zeige DUSP1 Antikörper) and Dusp4 (zeige DUSP9 Antikörper) are cardioprotective genes that play a critical role in the heart by dampening p38 MAPK (zeige MAPK14 Antikörper) signaling that would otherwise reduce contractility and induce cardiomyopathy.
Loss of MKP-2 regulates early inflammation in acute lung injury.
Increased DUSP4 (zeige DUSP9 Antikörper) expression in activated T cells in the elderly in part accounts for defective adaptive immune responses.
protein deficiency enhances CD25 (zeige IL2RA Antikörper) expression and CD4 (zeige CD4 Antikörper)+ T-cell proliferation without impeding T-cell development
The protein encoded by this gene is a member of the dual specificity protein phosphatase subfamily. These phosphatases inactivate their target kinases by dephosphorylating both the phosphoserine/threonine and phosphotyrosine residues. They negatively regulate members of the mitogen-activated protein (MAP) kinase superfamily (MAPK/ERK, SAPK/JNK, p38), which are associated with cellular proliferation and differentiation. Different members of the family of dual specificity phosphatases show distinct substrate specificities for various MAP kinases, different tissue distribution and subcellular localization, and different modes of inducibility of their expression by extracellular stimuli. This gene product inactivates ERK1, ERK2 and JNK, is expressed in a variety of tissues, and is localized in the nucleus. Two alternatively spliced transcript variants, encoding distinct isoforms, have been observed for this gene. In addition, multiple polyadenylation sites have been reported.
dual specificity protein phosphatase 4
, dual specificity phosphatase 4
, MAP kinase phosphatase 2
, VH1 homologous phosphatase 2
, dual specificity protein phosphatase hVH2
, mitogen-activated protein kinase phosphatase 2
, serine/threonine specific protein phosphatase