Only in Titles

           Search results for: Anti-DCK(deoxycytidine kinase) Antibody   

paperclip

#28945228   2017/09/25 Save this To Up

ERK-dependent IL-6 autocrine signaling mediates adaptive resistance to pan-PI3K inhibitor BKM120 in head and neck squamous cell carcinoma.

Hyperactivation of phosphatidylinositol 3-kinase (PI3K) pathway occurs frequently in head and neck squamous cell carcinoma (HNSCC). However, clinical outcomes of targeting the PI3K pathway have been underwhelming. In present study, we investigated the resistant mechanisms and potential combination therapeutic strategy to overcome adaptive resistance to PI3K inhibitor in HNSCC. Treatment of NVP-BKM120, a pan-PI3K inhibitor, led to upregulation of interleukin-6 (IL-6) and subsequent activation of either extracellular signal-regulated kinase (ERK) or signal transducers and activators of transcription 3 (STAT3), causing modest antitumor effects on the growth of HNSCC cells. Blockade of autocrine IL-6 signaling with siRNA or neutralizing antibody for IL-6 receptor (IL-6R) completely abolished NVP-BKM120-induced activation of ERK and STAT3 as well as expression of c-Myc oncogene, which resulted in enhanced sensitivity to NVP-BKM120. Moreover, when compared with a pharmacologic inhibitor or silencing of STAT3, trametinib, a MEK inhibitor, in combination with NVP-BKM120 yielded more potent anti-proliferative effects by inhibiting S phase transition, arresting cells at G0/G1 phase, and downregulating IL-6 and c-Myc expression. Furthermore, as compared with either agent alone, combination of NVP-BKM120 with trametinib or tocilizumab, a humanized anti-IL-6R antibody, significantly suppressed tumor growth in NVP-BKM120-resistant patient-derived tumor xenograft (PDTX) models, which was also confirmed in PDTX-derived cell lines. Collectively, these results suggested that IL-6/ERK signaling is closely involved in adaptive resistance of NVP-BKM120 in HNSCC cells, providing a rationale for a novel combination therapy to overcome resistance to PI3K inhibitors.Oncogene advance online publication, 25 September 2017; doi:10.1038/onc.2017.339.

2184 related Products with: ERK-dependent IL-6 autocrine signaling mediates adaptive resistance to pan-PI3K inhibitor BKM120 in head and neck squamous cell carcinoma.

Head and neck squamous ce Multiple head and neck sq Oral cavity squamous cell Oral squamous cell cancer Multiple organ squamous c Lung squamous cell carcin Esophagus squamous cell c Esophagus squamous cell c Esophagus squamous cell c Lung squamous cell carcin Lung squamous cell carcin Lung squamous cell carcin

Related Pathways

paperclip

#28944826   2017/09/25 Save this To Up

MACC‑1 antibody target therapy suppresses growth and migration of non‑small cell lung cancer.

Non‑small‑cell lung cancer (NSCLC) accounts for ~80% of human lung cancers that result in mortalities worldwide. Metastasis‑associated in colon cancer‑1 (MACC‑1) has been demonstrated to be significantly expressed in cases of NSCLC and promotes tumor cell migration and metastasis through transactivation of the metastasis‑inducing hepatocyte growth factor/MET proto‑gene, receptor tyrosine kinase (HGF/MET) signaling pathway. The present study constructed a chimeric antibody (Chanti‑MACC‑1) targeting MACC‑1 and investigated its potential as a molecular therapeutic target in the treatment of NSCLC therapy. The expression of MACC‑1 was detected by reverse transcription‑quantitative polymerase chain reaction and western blotting in lung cancer cell lines and tissues. MTT assay was used to detect proliferation of A549 cells treated by Chanti‑MACC‑1, whereas the functional and regulatory effects of Chanti‑MACC‑1 in the migration and metastasis of NSCLC cells was investigated by a cell invasion assay. The therapeutic effect and survival time was observed in animal models. The results demonstrated that MACC‑1 expression was increased and overexpression of MACC‑1 promoted the progression of the cell cycle, significantly promoted NSCLC cell growth and enhanced tumor migration and invasion through the HGF/MET signaling pathway. It was further demonstrated that Chanti‑MACC‑1 efficiently suppressed MACC‑1 expression and significantly inhibited NSCLC cell proliferation, migration and invasion by blocking the HGF/MET signaling pathway. The data revealed that Chanti‑MACC‑1 was not only beneficial for tumor remission, however additionally contributed to the long‑term survival of NSCLC ‑bearing mice. The findings of the present study indicated that MACC‑1 was significantly upregulated and promoted tumor cell growth and migration in NSCLC cells and tissues via transactivation of the metastasis‑inducing HGF/MET signaling pathway. However, Chanti‑MACC‑1significantly inhibited tumor growth and metastasis, which suggested that MACC‑1 may be essential for tumor initiation and progression by negatively regulating tumor suppressors.

2685 related Products with: MACC‑1 antibody target therapy suppresses growth and migration of non‑small cell lung cancer.

Small cell lung carcinoma Non small cell lung carci Lung non small cell cance Non small cell lung carci Lung small cell carcinoma Non small cell lung carci Non small cell lung carci High density non small ce Middle advanced stage lun Non small cell lung carci Non-small cell lung cance Anti C Reactive Protein A

Related Pathways

paperclip

#28943470   2017/09/25 Save this To Up

Eosinophils release extracellular DNA traps in response to Aspergillus fumigatus.

Eosinophils mediate the immune response in different infection conditions. The release of extracellular DNA traps (ETs) by leukocytes has been described as an innate immune response mechanism that is relevant in many disorders including fungal diseases. Different stimuli induce human eosinophil ETs (EETs) release. Aspergillus fumigatus (A. fumigatus) is an opportunistic fungus that may cause eosinophilic allergic bronchopulmonary aspergillosis (ABPA). It has been reported that eosinophils are important to the clearance of A. fumigatus in infected mice lungs. However, the immunological mechanisms that underlie the molecular interactions between A. fumigatus and eosinophils are poorly understood.

1305 related Products with: Eosinophils release extracellular DNA traps in response to Aspergillus fumigatus.

DNA (cytosine 5) methyltr Rat TGF-beta-inducible ea Rat TGF-beta-inducible ea Recombinant Human Interfe Native Influenza HA (A To Native Influenza HA (A To Native Influenza HA (A To Cell Meter™ Fluorimetri Cell Meter™ Fluorimetri Beta Amyloid (42) ELISA K Beta Amyloid (1 40) ELISA Beta Amyloid (40) ELISA K

Related Pathways

paperclip

#28943410   2017/09/25 Save this To Up

Loss of Reelin protects mice against arterial thrombosis by impairing integrin activation and thrombus formation under high shear conditions.

Reelin is a secreted glycoprotein and essential for brain development and plasticity. Recent studies provide evidence that Reelin modifies platelet actin cytoskeletal dynamics. In this study we sought to dissect the contribution of Reelin in arterial thrombus formation. Here we analyzed the impact of Reelin in arterial thrombosis ex vivo and in vivo using Reelin deficient (reeler) and wildtype mice. We found that Reelin is secreted upon platelet activation and mediates signaling via glycoprotein (GP)Ib, the amyloid precursor protein (APP) and apolipoprotein E receptor 2 (ApoER2) to induce activation of Akt, extracellular signal-regulated kinase (Erk), SYK and Phospholipase Cγ2. Moreover, our data identifies Reelin as first physiological ligand for platelet APP. Platelets from reeler mice displayed attenuated platelet adhesion and significantly reduced thrombus formation under high shear conditions indicating an important role for Reelin in GPIb-dependent integrin αIIbβ3 activation. Accordingly, adhesion to immobilized vWF as well as integrin activation and the phosphorylation of Erk and Akt after GPIb engagement was reduced in Reelin deficient platelets. Defective Reelin signaling translated into protection from arterial thrombosis and cerebral ischemia/reperfusion injury beside normal hemostasis. Furthermore, treatment with an antagonistic antibody specific for Reelin protects wildtype mice from occlusive thrombus formation. Mechanistically, GPIb co-localizes to the major Reelin receptor APP in platelets suggesting that Reelin-induced effects on GPIb signaling are mediated by APP-GPIb interaction. These results indicate that Reelin is an important regulator of GPIb-mediated platelet activation and may represent a new therapeutic target for the prevention and treatment of cardio- and cerebrovascular diseases.

1032 related Products with: Loss of Reelin protects mice against arterial thrombosis by impairing integrin activation and thrombus formation under high shear conditions.

Cytokeratin, High Molecu Cytokeratin, High Molecu Cytokeratin, High Molecu Cytokeratin, High Molecu Cytokeratin, High Molecu Cytokeratin, High Molecu DAB Chromogen Substrate DAB Substrate (High Cont DAB Substrate (High Cont DAB Substrate (High Cont DAB Chromogen Substrate DAB Chromogen Substrate

Related Pathways

paperclip

#28942884   2017/09/25 Save this To Up

Overexpression of IL-38 protein in anticancer drug-induced lung injury and acute exacerbation of idiopathic pulmonary fibrosis.

Interleukin (IL)-38, a member of the IL-1 family, shows high homology to IL-1 receptor antagonist (IL-1Ra) and IL-36 receptor antagonist (IL-36Ra). Its function in interstitial lung disease (ILD) is still unknown.

2567 related Products with: Overexpression of IL-38 protein in anticancer drug-induced lung injury and acute exacerbation of idiopathic pulmonary fibrosis.

Human Epstein-Barr Virus Mouse Epstein-Barr Virus Bovine prolactin-induced HIV 1 intergase antigen. Anti AGO2 Human, Monoclon Anti AGO2 Mouse, Monoclon Anti AGO2 Human, Monoclon Anti AGO2 Mouse, Monoclon CELLKINES Natural Human I Human Interleukin-4 IL-4 Human Interleukin-6 IL-6 Human Interleukin-7 IL-7

Related Pathways

paperclip

#28939820   2017/09/23 Save this To Up

Identification and characterisation of lamprey protein kinase C delta-like gene.

Protein kinase C-δ (PKC-δ), a member of the lipid-regulated serine/threonine PKC family, has been implicated in a wide range of important cellular processes, such as cell growth, differentiation, and apoptosis. Lampreys belong to the most primitive class of vertebrates, and there is little information on PKC-δ in these animals. In this study, a PKC-δ-like cDNA sequence and deduced PKC-δ-like amino acid sequence were identified in the Japanese lamprey (Lampetra japonica). The PKC-δ-like gene shared approximately 60% sequence identity with its homologs in jawed vertebrates. The anti-PKC-δ-like polyclonal antibodies were well prepared, and experiments showed that PKC-δ-like was primarily distributed in the supraneural body of the lamprey. Both mRNA and protein levels of PKC-δ-like in supraneural body cells were increased after incubation with cis-diaminedichloroplatinum (CDDP). Moreover, PKC-δ-like protein induced the apoptosis of HEK-293T cells. In addition, the activation of PKC-δ-like resulted in apoptosis. Conversely, the inhibition of PKC-δ-like activity disrupted the CDDP-mediated induction of cellular apoptosis. These results indicate that PKC-δ-like identified in lampreys might play an important role in apoptosis in jawless vertebrates.

2910 related Products with: Identification and characterisation of lamprey protein kinase C delta-like gene.

MIC2 Gene Protein, CD99; MIC2 Gene Protein, CD99; MIC2 Gene Protein, CD99; Protein Phosphatase 1 sub Rabbit Anti-IEX1 Differen Rabbit Anti-IEX1 Differen Rabbit Anti-IEX1 Differen Rabbit Anti-IEX1 Differen Rabbit Anti-IEX1 Differen Rabbit Anti-IEX1 Differen Rabbit Anti-IEX1 Differen Rabbit Anti-IEX1 Differen

Related Pathways

paperclip

#28939767   2017/09/23 Save this To Up

Dopamine Transporter Phosphorylation Site Threonine 53 is Stimulated by Amphetamines and Regulates Dopamine Transport, Efflux, and Cocaine Analog Binding.

The dopamine transporter (DAT) controls the spatial and temporal dynamics of dopamine neurotransmission through reuptake of extracellular transmitter and is a target for addictive compounds such as cocaine, amphetamine (AMPH), and methamphetamine (METH). Reuptake is regulated by kinase pathways and drug exposure, allowing for fine-tuning of clearance in response to specific conditions, and here we examine the impact of transporter ligands on DAT residue Thr53, a proline-directed phosphorylation site previously implicated in AMPH-stimulated efflux mechanisms. Our findings show that Thr53 phosphorylation is stimulated in a transporter-dependent manner by AMPH and METH in model cells and rat striatal synaptosomes, and in striatum of rats given subcutaneous injection of METH. Rotating disc electrode voltammetry revealed that initial rates of uptake and AMPH-induced efflux were elevated in phosphorylation-null T53A DAT relative to WT and charge-substituted T53D DATs, consistent with functions related to charge or polarity. These effects occurred without alterations of surface transporter levels, and mutants also showed reduced cocaine analog binding affinity that was not rescued by Zn(2+) Together these findings support a role for Thr53 phosphorylation in regulation of transporter kinetic properties that could impact DAT responses to amphetamines and cocaine.

2718 related Products with: Dopamine Transporter Phosphorylation Site Threonine 53 is Stimulated by Amphetamines and Regulates Dopamine Transport, Efflux, and Cocaine Analog Binding.

Dopamine antibody, Monocl Rat Anti-Human Dopamine T Rabbit Anti-Human Dopamin Rabbit Anti-Human Dopamin Rabbit Anti-Rat Androgen Rabbit Anti-Dopamine D2 R Rabbit Anti-Dopamine D2 R Anti-DAT(Sodium-dependent Anti DAT(Sodium dependent Anti-Dopamine Transporter Anti-Dopamine Transporter Androgen Receptor (Phosph

Related Pathways

paperclip

#28939348   2017/09/23 Save this To Up

Transcranial ultrasound stimulation promotes brain-derived neurotrophic factor and reduces apoptosis in a mouse model of traumatic brain injury.

The protein expressions of brain-derived neurotrophic factor (BDNF) can be elevated by transcranial ultrasound stimulation in the rat brain.

1440 related Products with: Transcranial ultrasound stimulation promotes brain-derived neurotrophic factor and reduces apoptosis in a mouse model of traumatic brain injury.

Monoclonal Anti-Brain-der Monoclonal Anti Brain der Anti-Human Brain-Derived Anti Human Brain Derived Brain Derived Neurotrophi Human Brain Derived Neuro Dog Brain-derived neurotr ELISA Kit for Brain Deriv Brain derived Neurotrophi Brain Derived Neurotrophi Mouse Stromal Cell-Derive Mouse Platelet Derived Gr

Related Pathways

paperclip

#28939254   2017/09/23 Save this To Up

Inhibition of MEK-ERK1/2-MAP kinase signalling pathway reduces rabies virus induced pathologies in mouse model.

The extracellular signal-regulated kinase (ERK) pathway has been shown to regulate pathogenesis of many viral infections, but its role during rabies virus (RV) infection in vivo is not clear. In the present study, we investigated the potential role of MEK-ERK1/2 signalling pathway in the pathogenesis of rabies in mouse model and its regulatory effects on pro-inflammatory cytokines and other mediators of immunity, and kinetics of immune cells. Mice were infected with 25 LD50 of challenge virus standard (CVS) strain of RV by intracerebral (i.c.) inoculation and were treated i.c. with U0126 (specific inhibitor of MEK1/2) at 10 μM/mouse at 0, 2, 4 and 6 days post-infection. Treatment with U0126 resulted in delayed disease development and clinical signs, increased survival time with lesser mortality than untreated mice. The better survival of inhibitor-treated and RV infected mice was positively correlated with reduced viral load and reduced viral spread in the brain as by quantified by real-time PCR, direct fluorescent antibody test and immunohistochemistry. CVS-infected/mock-treated mice developed severe histopathological lesions with increased Fluoro-Jade B positive degenerating neurons in brain, which were associated with higher levels of serum nitric oxide, iNOS, TNF-α, and CXCL10 mRNA. Also CVS-infected/U0126-treated mice revealed significant decrease in caspase 3 but increase in Bcl-2 mRNA levels and less TUNEL positive apoptotic cells. CVS-infected/U0126-treated group also showed significant increase in CD4(+), CD8(+) T lymphocytes and NK cells in blood and spleen possibly due to less apoptosis of these cells. In conclusion, these data suggest that MEK-ERK1/2 signalling pathway play critical role in the pathogenesis of RV infection in vivo and opens up new avenues of therapeutics.

2424 related Products with: Inhibition of MEK-ERK1/2-MAP kinase signalling pathway reduces rabies virus induced pathologies in mouse model.

Mouse Epstein-Barr Virus PathwayReady™ MAP Kinas Anti AGO2 Mouse, Monoclon Anti AGO2 Mouse, Monoclon Human Epstein-Barr Virus GPCR Signaling to MAPK ER MAPK Phospho-Specific Arr Human Mouse Rat Phospho-E Mouse Anti-Rabies Virus A Mouse Anti-Rabies Virus Mouse AntiInfluenza B Nuc Mouse Anti-Lipoprotein Li

Related Pathways

paperclip

#28928935   2017/09/22 Save this To Up

Case Report: Whole exome sequencing identifies a novel frameshift insertion c.1325dupT (p.F442fsX2) in the tyrosine kinase domain of BTK gene in a young Indian individual with X-linked agammaglobulinemia.

X-linked agammaglobulinemia (XLA) is an extremely rare inherited primary immunodeficiency characterized by recurrent bacterial infections, decrease in number of mature B cells and low serum immunoglobulins. XLA is caused by mutations in the gene encoding Bruton's tyrosine kinase. We report a case of a young Indian boy suspected to have XLA. Immunophenotyping was performed for the affected child using CD20, CD19 and CD3 antibodies. Whole exome sequencing was performed using trio-based approach. The variants were further analyzed using capillary sequencing in the trio as well as maternal grandmother. Initial immunophenotyping in the affected child showed decreased count of CD19+ B cells. To strengthen the clinical findings and confirm the diagnosis of XLA, we performed whole exome sequencing. Our analysis identified a novel frameshift insertion (c.1325dupT) in the BTK gene, which was further validated by Sanger sequencing. Our approach shows the potential in using whole exome sequencing to pinpoint the molecular lesion, enabling timely diagnosis and genetic counseling, and potentially offering prenatal genetic testing for the family.

2580 related Products with: Case Report: Whole exome sequencing identifies a novel frameshift insertion c.1325dupT (p.F442fsX2) in the tyrosine kinase domain of BTK gene in a young Indian individual with X-linked agammaglobulinemia.

Tyrosine Kinase Adaptors Goat Anti-Human Casein Ki FDA Standard Frozen Tissu FDA Standard Frozen Tissu FDA Standard Frozen Tissu FDA Standard Frozen Tissu FDA Standard Frozen Tissu FDA Standard Frozen Tissu Multiple organ tumor tiss DNA (cytosine 5) methyltr Aurora Kinase B Inhibitor Aurora Kinase B Inhibitor

Related Pathways

  •  
  • No related Items