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Mechanistically, nPAK4 promoted the metastasis of ERalpha-positive breast cancer cells by targeting LIFR, a bone metastasis suppressor. Strikingly, the nuclear accumulation of PAK4 might promote aggressive phenotypes, highlighting nPAK4 as a novel predictive biomarker for ERalpha-positive breast cancer bone metastasis.
PAK4-Slug axis represents a novel pathway that promotes PC progression
The authors demonstrated that the CDK2-PAK4 kinase signature may be a useful prognostic indicator and potential target for non-small cell lung cancers, and also proposed that poor outcome subgroup stratified by this classifier may benefit from the recently developed CDK2 and PAK4 inhibitors.
The apoptosis was partially dependent upon caspase-8 concomitant with attenuated NF-kappa B survival signal due to stimulus of TNF-alpha. It suggests that PAK4 as target is a switch between caspase-8 apoptosis and NF-kappa B survival signals induced by TNF-alpha in hepatocarcinoma cells.
These results implicate a novel role for PAK4 within the PI3K pathway via interaction with p85alpha. Thus, PAK4 could be an essential player in PDAC progression representing an interesting therapeutic opportunity.
This review will discuss the emerging data highlighting the prominence of PAK4 in Pancreatic distal adenocarcinoma(PDAC) and its potential role for transforming patient management.
this series of compounds has the potential for further development as PAK4 inhibitors for anticancer activity
X-ray crystallography reveals that in addition to the canonical PAK4 CDC42/RAC interactive binding (CRIB) domain binding to CDC42 there are unexpected contacts involving the PAK4 kinase C-lobe, CDC42, and the PAK4 polybasic region.
High PAK4 expression is associated with glioma.
These results indicate that miR485 acts as a tumour suppressor in Glioblastoma (GBM) by, at least partially, directly targeting PAK4 and regulating the AKT and ERK signalling pathways. Thus, miR485 may be a potential target for the treatment of patients with GBM.
Study reports the overexpression of PAK4 in neuroblastoma cells and, that PF-3758309, a potent PAK4 inhibitor, inhibits cell proliferation and survival in neuroblastoma cells via inhibition of the MEK/ERK pathway. These results suggest a role of PAK4 in neuroblastoma development.
Methylation at cg14010619 may modify PAK4 activity, which has been implicated in cisplatin resistance in malignant cell lines
PAK4 downregulated the level of p21 and enhanced the activity of Akt as well. And we conclude that PAK4 acts as a regulator of cell cycle progression of vascular smooth muscle cells by mediating Akt signaling and controlling p21 levels, which further modulate intimal hyperplasia and vascular smooth muscle cells proliferation
Findings revealed a novel function of PAK4 in thyroid stimulating hormone-induced papillary thyroid cancer progression.
The present study demonstrates that miR-145 plays an important role in inhibiting cell migration by directly targeting PAK4, and identifies miR-145-PAK4-LIMK1-cofilin as a novel regulatory pathway that contributed to colorectal cancer metastasis.
These findings revealed a novel glucose metabolism-related mechanism of PAK4 in promoting colon cancer cell growth, suggesting that PAK4 and/or G6PD blockage might be a potential therapeutic strategy for colon cancer.
PAK4 (but not PAK1) mediates invadopodia maturation during melanoma invasion likely via inhibition of PDZ-RhoGEF.
these results indicate that PAK4 confers CDDP resistance via the activation of MEK/ERK and PI3K/Akt pathways. PAK4 and PI3K/Akt pathways can reciprocally activate each other.
PAK4 activity was markedly decreased in postmortem brain tissue from Parkinson's disease (PD) patients and in rodent models of PD. Expression of constitutively active PAK4(S445N/S474E) (caPAK4) protected DA neurons in both the 6-hydroxydopamine and alpha-synuclein rat models of PD and preserved motor function.
Our results indicate that PAK4 plays an important role in the potentiation of insulin secretion by fatty acids downstream of GPR40.
Together, this suggests that PAK4 is dispensable for mouse pancreas development.
PAK4 crystal structures can be classified into specific conformational groups, and that these groups are associated with previously unobserved hinging motions and an unusual conformation for the kinase hydrophobic core. Our findings therefore indicate that there may be a diversity of kinase hinging motions, and that these may indicate different mechanisms of regulation.
PAK4 microparticles may have a role in the ventilation-induced lung injury process
These data demonstrate the relevance of PAK4 in osteoclast differentiation and the potential of PAK4 inhibitors for treating osteoclast-related disorders.
PAK4 promotes alpha-MSH/UVB-induced melanogenesis via the CREB and Wnt/beta-catenin signaling pathways and suggest that PAK4 may be a potential therapeutic target in pigmentation disorders.
PAK4 phosphorylates Par6B at Ser143 blocking its interaction with Cdc42.
Defined here is the overlap in phosphopeptides regulated by K-Ras, Cdc42, and PAK4; perturbation of these signaling components affects phosphoproteins associated with microtubule depolymerization, cytoskeletal organization, and the cell cycle.
These results indicate that PAK4 functions, including control of actin dynamics, are necessary for normal development of the heart
p21-activated kinase 4 regulates regulatory myosin light chain phosphorylation and myosin contractility during FcgammaR-mediated phagocytosis.
the transient increase in PAK4 levels at early G1 reduces p21 levels, thereby abrogating the activity of CDK4/CDK6 kinases, and allowing cells to proceed with the cell cycle in a precisely coordinated way
Conditional Pak4 knockout mice were born normally, but displayed growth retardation and died prematurely. The brains showed a dramatic decrease in proliferation of cortical and striatal neuronal progenitor cells.
results suggest that overexpression of Pak4 triggers events that are important for the transformation of mammary epithelial cells
PAK4 interacts with KGF receptor and mediate anti-apoptosis effects of KGF on epithelial cells.
PAK4 has a role in neural tube development
PAK4 can negatively regulate the activation of Rho through a direct protein-protein interaction with G protein-linked Rho GEFs
PAK4 mediates morphological changes through regulation of GEF-H1
Pak4-induced arrest is mediated by a pathway that requires the ERK mitogen-activated protein kinase, as well as the cell cycle inhibitors p16(INK4) and p19(ARF; expression levels are upregulated in response to stimuli that promote senescence
PAKs may represent a target for various neurotoxic protein oligomers, and signaling deficits may contribute to the behavioral defects in chronic neurodegenerative diseases.
Pak4 may play a vital role in a wide range of different types of cancer.
pneumolysin selectively induced expression of MKP1 via a TLR4-dependent MyD88-TRAF6-ERK pathway, which inhibited the PAK4-JNK signaling pathway,leading to up-regulation of MUC5AC mucin production
pak4 is dispensable in zebrafish.
Zebrafish pak4 is required for primitive myeloid cell development.
PAK proteins, a family of serine/threonine p21-activating kinases, include PAK1, PAK2, PAK3 and PAK4. PAK proteins are critical effectors that link Rho GTPases to cytoskeleton reorganization and nuclear signaling. They serve as targets for the small GTP binding proteins Cdc42 and Rac and have been implicated in a wide range of biological activities. PAK4 interacts specifically with the GTP-bound form of Cdc42Hs and weakly activates the JNK family of MAP kinases. PAK4 is a mediator of filopodia formation and may play a role in the reorganization of the actin cytoskeleton. Multiple alternatively spliced transcript variants encoding distinct isoforms have been found for this gene.
, p21(CDKN1A)-activated kinase 4
, p21-activated kinase 4
, protein kinase related to S. cerevisiae STE20, effector for Cdc42Hs
, serine/threonine-protein kinase PAK 4
, p21 (CDKN1A)-activated kinase 4
, p21 protein (Cdc42/Rac)-activated kinase 4