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#28456137   2017/04/29 Save this To Up

The association of severe encephalopathy and question mark ear is highly suggestive of loss of MEF2C function.

Auriculocondylar syndrome and isolated question mark ear result from dysregulation of the endothelin 1-endothelin receptor type A signaling pathway. Animal models have highlighted the role of the transcription factor MEF2C as an effector of this pathway. We report heterozygous MEF2C loss-of-function as a possible cause of question mark ear associated with intellectual deficiency.

2623 related Products with: The association of severe encephalopathy and question mark ear is highly suggestive of loss of MEF2C function.

Ofloxacin CAS Number [824 Rabbit Anti-Tyrosine Hydr Rabbit Anti-Tyrosine Hydr Rabbit Anti-Tyrosine Hydr Rabbit Anti-Tyrosine Hydr Rabbit Anti-Tyrosine Hydr Rabbit Anti-Tyrosine Hydr Rabbit Anti-gamma tubulin Rabbit Anti-gamma tubulin Rabbit Anti-gamma tubulin Rabbit Anti-gamma tubulin Rabbit Anti-gamma tubulin

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#28456097   2017/04/29 Save this To Up

Structure-guided cancer blockade between bioactive bursehernin and proteins: Molecular docking and molecular dynamics study.

Bursehernin (5'-desmethoxyyatein) is a natural lignan, which has anti-tumor activity in vitro. In this study, the binding-inhibitory effects of bursehernin were screening on selected 80 proteins associated with cancer pathway. The computational analysis suggested inhibitory effect due to bursehernin towards proteins related to cancer proliferation, including FMS kinase receptor, heat shock protein 90-α (Hsp90-α), adenylate cyclase 10 (ADCY10), mitogen-activated protein kinase kinase (MEK1), and α-tubulin. Moreover, bursehernin could interfere with cell cycle progression via binding to cyclin B proteins. Among all screened proteins, the compound showed an interesting binding affinity to the FMS kinase receptor. The binding mode studies by molecular dynamic technique showed that aromatic ring of bursehernin compound was responsible for compound-protein interaction through pi-pi stacking with Tyr105 and Phe178 of the FMS kinase receptor. This study suggests that bursehernin has potential for development as an anti-tumor agent with an anti-proliferation, and cell cycle arrest inducing, although further studies are needed.

2079 related Products with: Structure-guided cancer blockade between bioactive bursehernin and proteins: Molecular docking and molecular dynamics study.

Plasma Proteins: Two Chai Recombinant Human Androge Cytokeratin, High Molecu Cytokeratin, High Molecu Cytokeratin, High Molecu Cytokeratin, High Molecu Cytokeratin, High Molecu Cytokeratin, High Molecu Growth Differentiation Fa Androgen Receptor (Phosph Androgen Receptor (Phosph Rabbit Anti-Human Androge

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#28456096   2017/04/29 Save this To Up

Identifying low density lipoprotein cholesterol associated variants in the Annexin A2 (ANXA2) gene.

Annexin-A2 (AnxA2) is an endogenous inhibitor of proprotein convertase subtilisin/kexin type-9 (PCSK9). The repeat-one (R1) domain of AnxA2 binds to PCSK9, blocking its ability to promote degradation of low-density lipoprotein cholesterol-receptors (LDL-R) and thereby regulate low-density lipoprotein cholesterol (LDL-C) levels. Here we identify variants in ANXA2 influencing LDL-C levels and we determine the molecular mechanisms of their effects.

2178 related Products with: Identifying low density lipoprotein cholesterol associated variants in the Annexin A2 (ANXA2) gene.

Low Density Lipoprotein Low Density Lipoprotein Low Density Lipoprotein Primary antibody low den Lipoprotein, Human Plasma Lipoproteins, Human Plasm Lipoproteins, Human Plasm Mouse Anti-Human Low Dens Low density malignant mel DNA (cytosine 5) methyltr Human Epstein-Barr Virus Mouse Epstein-Barr Virus

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#28456063   2017/04/29 Save this To Up

Ocular findings in adult subjects with an inactivating mutation in GH releasing hormone receptor gene.

Ocular function is fundamental for environmental adaptation and survival capacity. Growth factors are necessary for a mature eyeball, needed for adequate vision. However, the consequences of the deficiency of circulating growth hormone (GH) and its effector insulin-like growth factor I (IGF-I) on the physical aspects of the human eye are still debated. A model of untreated isolated GH deficiency (IGHD), with low but measurable serum GH, may clarify this issue. The aim of this study was to assess the ocular aspects of adult IGHD individuals who have never received GH therapy.

1303 related Products with: Ocular findings in adult subjects with an inactivating mutation in GH releasing hormone receptor gene.

Interferon-a Receptor Typ Mouse Anti-Human Interleu interleukin 17 receptor C interferon-alpha receptor Anti beta3 AR Human, Poly IGF-1R Signaling Phospho- Insulin Receptor Phospho- Nuclear Membrane Receptor T-Cell Receptor Signaling Rabbit Anti-Insulin Recep Rabbit Anti-Insulin Recep Rabbit Anti-Insulin Recep

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#28456019   2017/04/29 Save this To Up

Dual host specificity of phage SP6 is facilitated by tailspike rotation.

Bacteriophage SP6 exhibits dual-host adsorption specificity. The SP6 tailspikes are recognized as important in host range determination but the mechanisms underlying dual host specificity are unknown. Cryo-electron tomography and sub-tomogram classification were used to analyze the SP6 virion with a particular focus on the interaction of tailspikes with host membranes. The SP6 tail is surrounded by six V-shaped structures that interconnect in forming a hand-over-hand hexameric garland. Each V-shaped structure consists of two trimeric tailspike proteins: gp46 and gp47, connected through the adaptor protein gp37. SP6 infection of Salmonella enterica serovars Typhimurium and Newport results in distinguishable changes in tailspike orientation, providing the first direct demonstration how tailspikes can confer dual host adsorption specificity. SP6 also infects S. Typhimurium strains lacking O antigen; in these infections tailspikes have no apparent specific role and the phage tail must therefore interact with a distinct host receptor to allow infection.

2236 related Products with: Dual host specificity of phage SP6 is facilitated by tailspike rotation.

MOUSE ANTI BOVINE ROTAVIR MOUSE ANTI BORRELIA BURGD NATIVE HUMAN PROLACTIN, P RABBIT ANTI GSK3 BETA (pS 10x ELISA WASH BUFFER, Pr 10X PHOSPHATE BUFFERED SA PERMANENT AQUEOUS MOUNTIN MOUSE ANTI CANINE DISTEMP MOUSE ANTI HUMAN CD15, Pr NATIVE HUMAN PROLACTIN, P MOUSE ANTI HUMAN CD19 RPE MOUSE ANTI HUMAN CD15, Pr

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#28456011   2017/04/29 Save this To Up

Neurosteroid biosynthesis downregulation and changes in GABAA receptor subunit composition: A biomarker axis in stress-induced cognitive and emotional impairment.

By rapidly modulating neuronal excitability, neurosteroids regulate physiological processes, such as responses to stress and development. Excessive stress affects their biosynthesis and causes an imbalance in cognition and emotions. The progesterone derivative, allopregnanolone (Allo) enhances extrasynaptic and postsynaptic inhibition by directly binding at GABAA receptors, and thus, positively and allosterically modulates the function of GABA. Allo levels are decreased in stress-induced psychiatric disorders, including depression and post-traumatic stress disorder (PTSD), and elevating Allo levels may be a valid therapeutic approach to counteract behavioural dysfunction. While benzodiazepines are inefficient, selective serotonin reuptake inhibitors (SSRIs) represent the first choice treatment for depression and PTSD. Their mechanisms to improve behaviour in preclinical studies include neurosteroidogenic effects at low non-serotonergic doses. Unfortunately, half of PTSD and depressed patients are resistant to current prescribed "high" dosage of these drugs that engage serotonergic mechanisms. Unveiling novel biomarkers to develop more efficient treatment strategies is in high demand. Stress-induced downregulation of neurosteroid biosynthesis and changes in GABAA receptor subunit expression offer a putative biomarker axis to develop new PTSD treatments. The advantage of stimulating Allo biosynthesis relies on the variety of neurosteroidogenic receptors to be targeted, including TSPO and endocannabinoid receptors. Furthermore, stress favours a GABAA receptor subunit composition with higher sensitivity for Allo. The use of synthetic analogues of Allo is a valuable alternative. Pregnenolone or drugs that stimulate its levels increase Allo but also sulphated steroids, including pregnanolone sulphate which, by inhibiting NMDA tonic neurotransmission, provides neuroprotection and cognitive benefits. In this review we describe current knowledge on the effects of stress on neurosteroid biosynthesis and GABAA receptor neurotransmission and summarize available pharmacological strategies that by enhancing neurosteroidogenesis are relevant for the treatment of SSRI-resistant patients.

1293 related Products with: Neurosteroid biosynthesis downregulation and changes in GABAA receptor subunit composition: A biomarker axis in stress-induced cognitive and emotional impairment.

Interferon-a Receptor Typ ELISA Human , Interleukin Anti AGO2 Human, Monoclon Anti AGO2 Mouse, Monoclon Anti AGO2 Human, Monoclon Anti AGO2 Mouse, Monoclon Androgen Receptor (Phosph Androgen Receptor (Phosph Mouse Anti-Human Interleu Rabbit Anti-Human Androge Rabbit Anti-Human Androge Androgen Receptor (Ab 650

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#28455988   2017/04/29 Save this To Up

A genome-wide microRNA profiling indicates miR-424-5p and miR-503-5p as regulators of ALK expression in neuroblastoma.

The discovery of missense mutations of ALK gene identified this receptor tyrosine kinase as a therapeutic target in neuroblastoma (NB). Moreover, a high level of ALK protein has been associated with metastatic NB cases and with a worse prognosis, suggesting that also ALK overexpression is involved in NB tumorigenesis. Since miRNAs play key roles in the regulation of gene expression we aimed at identifying those miRNAs that can regulate ALK in NB. We therefore analyzed the genome-wide expression profile of miRNAs in two sample sets of 16 NB cell lines and 22 NB samples by using miRNA microarrays. Both sample sets were then divided into two subgroups showing high (ALK+) or low/absent (ALK-) expression of ALK. Results showed a down-regulation of 30 and 23 miRNAs (p-value <0.05) in the ALK+ group in NB cell lines and samples, respectively. Validation analysis indicated that miR-424-5p and miR-503-5p, belonging to the same cluster, were differentially expressed in both NB cell lines and tumor samples. Although only miR-424-5p showed a direct binding to ALK 3'-UTR, both miRNAs led to a remarkable decreasing of ALK protein as well as to the inhibition of cell viability in ALK+ NB cell lines. In conclusion, our data indicate that both miR-424-5p and miR-503-5p are involved in regulating ALK expression in NB, either by directly targeting ALK receptor or indirectly, and may thus serve as potential therapeutic tools in ALK dependent NBs.

2589 related Products with: A genome-wide microRNA profiling indicates miR-424-5p and miR-503-5p as regulators of ALK expression in neuroblastoma.

Amplite™ Fluorimetric A Alkaline Phospatase (ALP) ASP-3026 Mechanisms: ALK miRZip 106a anti miR 106a Anti AGO2 Human, Monoclon Anti AGO2 Mouse, Monoclon Anti AGO2 Human, Monoclon Anti AGO2 Mouse, Monoclon DNA (cytosine 5) methyltr EMAP-II Inhibitor Z-ASTD- EMAP-II Inhibitor Z-ASTD- EMAP II Inhibitor Z ASTD

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#28455978   2017/04/29 Save this To Up

N-Acetylcysteine breaks resistance to trastuzumab caused by MUC4 overexpression in human HER2 positive BC-bearing nude mice monitored by 89Zr-Trastuzumab and 18F-FDG PET imaging.

Trastuzumab remains an important drug in the management of human epidermal growth factor receptor 2 (HER2) overexpressing breast cancer (BC). Several studies reported resistance mechanisms to trastuzumab, including impaired HER2-accessibility caused by mucin 4 (MUC4). Previously, we demonstrated an increase of Zirconium-89-radiolabeled-trastuzumab (89Zr-Trastuzumab) accumulation when MUC4-overexpressing BC-cells were challenged with the mucolytic drug N-Acetylcysteine (NAC). Hereby, using the same approach we investigated whether tumor exposure to NAC would also enhance trastuzumab-efficacy.Dual SKBr3 (HER2+/MUC4-, sensitive to trastuzumab) and JIMT1 (HER2+/MUC4+, resistant to trastuzumab) HER2-BC-bearing-xenografts were treated with trastuzumab and NAC. Treatment was monitored by molecular imaging evaluating HER2-accessibility/activity (89Zr-Trastuzumab HER2-immunoPET) and glucose metabolism (18F-FDG-PET/CT), as well as tumor volume and the expression of key proteins.In the MUC4-positive JIMT1-tumors, the NAC-trastuzumab combination resulted in improved tumor-growth control compared to trastuzumab alone; with smaller tumor volume/weight, lower 18F-FDG uptake, lower %Ki67 and pAkt-expression. NAC reduced MUC4-expression, but did not affect HER2-expression or the trastuzumab-sensitivity of the MUC4-negative SKBr3-tumors.These findings suggest that improving HER2-accessibility by reducing MUC4-masking with the mucolytic drug NAC, results in a higher anti-tumor effect of trastuzumab. This provides a rationale for the potential benefit of this approach to possibly treat a subset of HER2-positive BC overexpressing MUC4.

2272 related Products with: N-Acetylcysteine breaks resistance to trastuzumab caused by MUC4 overexpression in human HER2 positive BC-bearing nude mice monitored by 89Zr-Trastuzumab and 18F-FDG PET imaging.

Recombinant Human Interfe BYL-719 Mechanisms: PI3K- Goat Anti-Human TOM1L1 SR Rabbit Anti-Human Toll In Anti C Reactive Protein A Anti AGO2 Human, Monoclon Anti AGO2 Human, Monoclon CELLKINES Natural Human I Human Interleukin-4 IL-4 Human Interleukin-6 IL-6 Human Interleukin-7 IL-7 Human Interleukin-2 IL-2

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#28455963   2017/04/29 Save this To Up

TrkC promotes colorectal cancer growth and metastasis.

The current work reveals that TrkC receptor is crucial to many aspects of tumorigenicity and metastasis of cancer. However, with only a few exceptions, such as colorectal cancer (CRC), where suppressing tumorigenic and metastatic ability via expression of TrkC as tumor suppressor have been proposed. These diverse lines of evidence led us to investigate whether TrkC is involved in CRC progression. By using mouse models and molecular biology analyses, we demonstrate that TrkC acts as an activator in tumorigenicity and metastasis of colorectal cancer. In this study, TrkC was frequently overexpressed in CRC cells, patients' tumor samples and an azoxymethane/dextran sulphate sodium-induced mouse model of colitis-associated CRCs. TrkC expression was associated with a high-grade CRC phenotype, leading to significantly poorer survival. Also, TrkC expression promoted the acquisition of motility and invasiveness in CRC. Moreover, TrkC increased the ability to form tumor spheroids, a property associated with cancer stem cells. Importantly, knockdown of TrkC in malignant mouse or human CRC cells inhibited tumor growth and metastasis in a mouse xenograft model. Furthermore, TrkC enhanced metastatic potential and induced proliferation by aberrant gain of AKT activation and suppression of transforming growth factor (TGF)-β signalling. Interestingly, TrkC not only modulated the actions of TGF-β type II receptor, but also attenuated expression of this receptor. These findings reveal an unexpected physiological role of TrkC in the pathogenesis of CRC. Therefore, TrkC is a potential target for designing effective therapeutic strategies for CRC development.

1583 related Products with: TrkC promotes colorectal cancer growth and metastasis.

Colorectal (colon and rec Colorectal (colon and rec Colorectal cancer tissue Mid advanced stage bladde Breast cancer tissue arra Middle advanced stage bre Middle advanced stage bre Colorectal carcinoma and Colon cancer tissue array Mid advanced stage uterin Middle advanced stage eso Esophagus cancer with mat

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#28455962   2017/04/29 Save this To Up

RUNX1 and breast cancer.

News on: Runx1 stabilizes the mammary epithelial cell phenotype and prevents epithelial to mesenchymal transition, by Hong et al. Oncotarget. 2017; 8:17610-27. doi: 10.18632/oncotarget.15381.

1149 related Products with: RUNX1 and breast cancer.

Breast cancer membrane pr Breast cancer (multiple t Breast cancer tissue arra Breast cancer (IDC) tissu Breast cancer and adjacen Breast cancer tissue arra Breast cancer tissue arra Breast cancer tissue arra Breast cancer tissue arra Breast cancer and matched Breast cancer and matched Tissue microarray of brea

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