Only in Titles

           Search results for: miRNASelect™ pEGP_mmu_mir_770 Expression Vector   

paperclip

#29464079   // Save this To Up

Differential tumor biological role of the tumor suppressor KAI1 and its splice variant in human breast cancer cells.

The tetraspanin and tumor suppressor KAI1 is downregulated or lost in many cancers which correlates with poor prognosis. KAI1 acts via physical/functional crosstalk with other membrane receptors. Also, a splice variant of KAI1 (KAI1-SP) has been identified indicative of poor prognosis. We here characterized differential effects of the two KAI1 variants on tumor biological events involving integrin (αvß3) and/or epidermal growth factor receptor (EGF-R). In MDA-MB-231 and -435 breast cancer cells, differential effects were documented on the expression levels of the tumor biologically relevant integrin αvß3 which colocalized with KAI1-WT but not with KAI1-SP. Cellular motility was assessed by video image processing, including motion detection and vector analysis for the quantification and visualization of cell motion parameters. In MDA-MB-231 cells, KAI1-SP provoked a quicker wound gap closure and higher closure rates than KAI1-WT, also reflected by different velocities and average motion amplitudes of singular cells. KAI1-SP induced highest cell motion adjacent to the wound gap borders, whereas in MDA-MB-435 cells a comparable induction of both KAI1 variants was noticed. Moreover, while KAI1-WT reduced cell growth, KAI1-SP significantly increased it going along with a pronounced EGF-R upregulation. KAI1-SP-induced cell migration and proliferation was accompanied by the activation of the focal adhesion and Src kinase. Our findings suggest that splicing of KAI1 does not only abrogate its tumor suppressive functions, but even more, promotes tumor biological effects in favor of cancer progression and metastasis.

1953 related Products with: Differential tumor biological role of the tumor suppressor KAI1 and its splice variant in human breast cancer cells.

Breast tumor survey tissu Breast tumor survey tissu Breast tumor survey tissu Breast tumor survey tissu Breast tumor survey tissu Breast tumor survey tissu Breast tumor survey tissu Breast tumor survey tissu Breast tumor survey tissu Breast tumor survey tissu Breast tumor survey tissu Breast tumor survey tissu

Related Pathways

paperclip

#29464040   // Save this To Up

Activation of Grm1 expression by mutated BRaf (V600E)and.

Our laboratory previously showed that ectopic expression of Grm1 is sufficient to induce spontaneous melanoma formation with 100% penetrance in transgenic mouse model, TG-3, which harbors wild-type BRaf. Studies identified Grm1 expression in human melanoma cell lines and primary to secondary metastatic melanoma biopsies having wild-type or mutated BRaf, but not in normal melanocytes or benign nevi. Grm1 expression was detected in tissues from mice genetically engineered with inducible melanocyte-specific BRaf. Additionally, stable clones derived from introduction of exogenous BRafin mouse melanocytes also showed Grm1 expression, which was not detected in the parental or empty vector-derived cells, suggesting that expression of BRafcould activate Grm1 expression. Despite aberrant Grm1 expression in the inducible, melanocyte-specific BRafmice, no tumors formed. However, in older mice, the melanocytes underwent senescence, as demonstrated previously by others. It was proposed that upregulated p15 and TGFβ contributed to the senescence phenotype. In contrast, in older TG-3 mice the levels of p15 and TGFβ remained the same or lower. Taken together, these results suggest the temporal regulation on the expression of "oncogenes" such as Grm1 or BRafis critical in the future fate of the cells. If BRafis turned on first, Grm1 expression can be induced, but this is not sufficient to result in development of melanoma; the cells undergo senescence. In contrast, if ectopic expression of Grm1 is turned on first, then regardless of wild-type or mutated BRaf in the melanocytes melanoma development is the consequence.

2728 related Products with: Activation of Grm1 expression by mutated BRaf (V600E)and.

Expression Media Products Expression Media Products Expression Media Products DNA (cytosine 5) methyltr Stat3 Activation Inhibito EtBr Destaining Bag Kit A baculoCOMPLETE protein ex Expression Systems Cre Expression Plasmid 70 Cre Expression Plasmid 70 Gryphon™ Retroviral Exp Gene Expression: Mouse N

Related Pathways

paperclip

#29463827   // Save this To Up

Long non-coding RNA AC026166.2-001 inhibits cell proliferation and migration in laryngeal squamous cell carcinoma by regulating the miR-24-3p/p27 axis.

Long non-coding RNA (lncRNA) AC026166.2-001 was found to be down-regulated in laryngeal squamous cell carcinoma (LSCC) tissues and metastatic neck lymph nodes. Decreased AC026166.2-001 was associated with poorer prognosis and may act as a novel biomarker for LSCC patients. In this study, AC026166.2-001 was overexpressed by a lentivirus vector and down-regulated by a small interfering RNA (siRNA). The results of real-time cell analysis (RTCA) and a plate colony formation assay showed that AC026166.2-001 inhibited LSCC cell proliferation and the clone-forming capacity. Cell cycle distribution and related protein changes were measured by flow cytometry. AC026166.2-001 arrested the cell cycle at the G1 phase and induced apoptosis. In addition, AC026166.2-001 decreased cell migration as measured by wound healing assays and transwell migration assays. Moreover, luciferase reporter assay and Western blotting results suggested that AC026166.2-001 acts as a sponge of miR-24-3p and regulates the expression of p27 and cyclin D1. The in vivo results showed that AC026166.2-001 significantly suppressed the growth of LSCC xenografts and promoted apoptosis. We validated the molecular mechanisms underlying AC026166.2-001 in LSCC. This is the first report of AC026166.2-001 acting as a tumor suppressor in LSCC by regulating the miR-24-3p/p27 axis.

1142 related Products with: Long non-coding RNA AC026166.2-001 inhibits cell proliferation and migration in laryngeal squamous cell carcinoma by regulating the miR-24-3p/p27 axis.

Esophageal squamous cell Lung squamous cell carcin Head and neck squamous ce Cervix squamous cell carc Esophagus squamous cell c Esophagus squamous cell c Esophagus squamous cell c Esophageal squamous cell Kidney clear cell carcino Lung large cell carcinoma Laryngeal squamous cell c Oral cavity squamous cell

Related Pathways

paperclip

#29463653   // Save this To Up

Efficient and Scalable Precision Genome Editing inthrough Conditional Recombineering and CRISPR/Cas9-Mediated Counterselection.

is an important human pathogen, but studies of the organism have suffered from the lack of a robust tool set for its genetic and genomic manipulation. Here we report the development of a system for the facile and high-throughput genomic engineering ofusing single-stranded DNA (ssDNA) oligonucleotide recombineering coupled with clustered regularly interspaced short palindromic repeat (CRISPR)/Cas9-mediated counterselection. We identify recombinase, derived from, as being capable of integrating single-stranded DNA oligonucleotides into thegenome. We found thatcan readily mediate recombineering across multiple characterized strains (3 of 3 tested) and primary clinical isolates (6 of 6 tested), typically yielding thousands of recombinants per transformation. Surprisingly, we also found that somestrains are naturally recombinogenic at measurable frequencies when oligonucleotides are introduced by electroporation, even without exogenous recombinase expression. We construct a temperature-sensitive, two-vector system which enables conditional recombineering and CRISPR/Cas9-mediated counterselection inwithout permanently introducing exogenous genetic material or unintended genetic lesions. We demonstrate the ability of this system to efficiently and precisely engineer point mutations and large single-gene deletions in thegenome and to yield highly enriched populations of engineered recombinants even in the absence of an externally selectable phenotype. By virtue of utilizing inexpensive, commercially synthesized synthetic DNA oligonucleotides as substrates for recombineering and counterselection, this system provides a scalable, versatile, precise, inexpensive, and generally useful tool for producing isogenic strains inwhich will enable the high-throughput functional assessment of genome variation and gene function across multiple strain backgrounds.Engineering genetic changes in bacteria is critical to understanding the function of particular genes or mutations but is currently a laborious and technically challenging process to perform for the important human pathogenIn an effort to develop methods which are rapid, easy, scalable, versatile, and inexpensive, here we describe a system for incorporating synthetic, mutagenic DNA molecules into thegenome and for eliminating cells that lack the engineered mutation. This method allows efficient, precise, and high-throughput genetic engineering ofstrains and will facilitate studies seeking to address a variety of issues about the function of particular genes and specific mutations.

2991 related Products with: Efficient and Scalable Precision Genome Editing inthrough Conditional Recombineering and CRISPR/Cas9-Mediated Counterselection.

Androgen Receptor (Phosph Androgen Receptor (Phosph Rabbit Anti-Human Androge Rabbit Anti-Human Androge Androgen Receptor (Ab 650 AZD-3514 Mechanisms: Andr 17β-Acetoxy-2α-bromo-5 (5α,16β)-N-Acetyl-16-[2 (5α,16β)-N-Acetyl-16-ac 5α-N-Acetyl-2'H-androst- 5α-N-Acetyl-2'H-androst- 3-O-Acetyl 5,14-Androstad

Related Pathways

paperclip

#29463326   // Save this To Up

Functional characteristics of chemosensory proteins in the sawyer beetle Monochamus alternatus Hope.

The Japanese pine sawyer, Monochamus alternatus Hope (Coleoptera: Cerambycidae), is a major pest of pines and it is also the key vector of the exotic pinewood nematode in China. In the present study, we cloned, expressed, and purified a chemosensory protein (CSP) in M. alternatus. We surveyed its expression in various developmental stages of male and female adult tissues and determined its binding affinities for different pine volatiles using a competitive binding fluorescence assay. A CSP known as CSP5 in M. alternatus was obtained from an antennal cDNA library and expressed in Escherichia coli. Quantitative reverse transcription polymerase chain reaction results indicated that the CSP5 gene was mainly expressed in male and female antennae. Competitive binding assays were performed to test the binding affinity of recombinant CSP5 to 13 odour molecules of pine volatiles. The results showed that CSP5 showed very strong binding abilities to myrcene, (+)-β-pinene, and (-)-isolongifolene, whereas the volatiles 2-methoxy-4-vinylphenol, p-cymene, and (+)-limonene oxide have relatively weak binding affinity at pH 5.0. Three volatiles myrcene, (+)-β-pinene, and (-)-isolongifolene may play crucial roles in CSP5 binding with ligands but this needs further study for confirmation. The sensitivity of insect to host plant volatiles can effectively be used to control and monitor the population through mass trapping as part of integrated pest management programs.

2160 related Products with: Functional characteristics of chemosensory proteins in the sawyer beetle Monochamus alternatus Hope.

Native Influenza HA (A Br Native Influenza HA (A Br Native Influenza HA (A Br Native Influenza HA (A Ca Native Influenza HA (A Ca Native Influenza HA (A Ca Recombinant Influenza HA Recombinant Influenza HA Recombinant Influenza HA Native Influenza HA (B Fl Native Influenza HA (B Fl Native Influenza HA (B Fl

Related Pathways

paperclip

#29462293   // Save this To Up

Intrathecal gene therapy in mouse models expressing CMT1X mutations.

GJB1 gene mutations affecting the gap junction protein connexin32 (Cx32) cause the X-linked Charcot-Marie-Tooth disease (CMT1X), a common inherited neuropathy. Targeted expression of virally delivered Cx32 in Schwann cells following intrathecal injection of lentiviral vectors in the Cx32 knockout (KO) mouse model of the disease has led to morphological and functional improvement. To examine whether this approach could be effective in CMT1X patients expressing different Cx32 mutants, we treated transgenic Cx32 KO mice expressing the T55I, R75W or N175D CMT1X mutations. All three mutants were localized in the perinuclear compartment of myelinating Schwann cells consistent with retention in the ER (T55I) or Golgi (R75W, N175D) and loss of physiological expression in the non-compact myelin. Following intrathecal delivery of the GJB1 gene we detected the virally delivered wild-type (WT) Cx32 in non-compact myelin of T55I KO mice, but only rarely in N175D KO or R75W KO mice, suggesting dominant-negative effects of the R75W and N175D mutants but not of the T55I mutant on co-expressed WT Cx32. GJB1 treated T55I KO mice showed improved motor performance, lower ratios of abnormally myelinated fibers and reduction of inflammatory cells in spinal roots and peripheral nerves compared to mock-treated littermates. Either partial (N175D KO) or no (R75W KO) improvement was observed in the other two mutant lines. Thus, certain CMT1X mutants may interfere with gene addition therapy for CMT1X. Whereas gene addition can be used for non-interfering CMT1X mutations, further studies will be needed to develop treatments for patients harboring interfering mutations.

1021 related Products with: Intrathecal gene therapy in mouse models expressing CMT1X mutations.

Mouse Epstein-Barr Virus Sterile filtered mouse s Anti AGO2 Mouse, Monoclon Anti AGO2 Mouse, Monoclon HIV1 integrase antibody, DNA (cytosine 5) methyltr Human Epstein-Barr Virus Goat Anti-Mouse SAR1, (in Goat Anti-Mouse Rab17 (mo Goat Anti-Mouse IA2, (int Goat Anti-Human, Mouse HI Goat Anti-Human FTO (Mous

Related Pathways

paperclip

#29461605   // Save this To Up

MiR-210 protects cardiomyocytes from OGD/R injury by inhibiting E2F3.

To detect the change in miRNA-210 expression of cardiomyocytes under hypoxia/reoxygenation status. Also, the effect of miR-210 on the apoptosis of cardiomyocytes induced by oxygen-glucose deprivation/reperfusion (OGD/R) and its mechanism through establishing the OGD/R injury model of primary cardiomyocytes in this experiment were investigated.

1046 related Products with: MiR-210 protects cardiomyocytes from OGD/R injury by inhibiting E2F3.

Rabbit Anti-ATAD5 Polyclo Rabbit Anti-ATAD5 Polyclo B-Phycoerythrin antibody EZH2 KMT6 antibody Isoty Uroguanylin (1-8) antibo Uroguanylin antibody Hos Interleukin-34 IL34 (N-t Interleukin-34 IL34 anti ZBTB7B antibody Host rab ZBTB7C antibody Host rab SLC12A2 antibody Host ra SULF2 antibody Host rabb

Related Pathways

paperclip

#29458871   // Save this To Up

DNA sequence-specific dimeric bisbenzimidazoles DBP(n) and DBPA(n) as inhibitors of H-NS silencing in bacterial cells.

DNA sequence-specific fluorescent dimeric bisbenzimidazoles DBP(n) and DBPA(n), noncovalently interacting with A-T pairs in the minor groove of double-stranded DNA were used for studying and monitoring the expression of histone-like H-NS-dependent promoters. Histone-like H-NS selectively binds to AT-rich segments of DNA and silences a large number of genes in bacterial chromosomes. The H-NS-dependent promoters of Quorum Sensing (QS)-regulated lux operons of the marine bacteria mesophilic Aliivibrio fischeri, psychrophilic Aliivibrio logei were used. Escherichia coli lux biosensors were constructed by cloning fragments bearing QS-regulated promoters into the vector, thereby placing each fragment upstream of the promoterless Photorhabdus luminescens luxCDABE genes. It was shown that the dimeric bisbenzimidazoles DBP(n) and DBPA(n) counteract the H-NS silencing activity. Thus, the presence of DBP(n) or DBPA(n) in the medium leads to an approximately 10-100-fold increase in the level of transcription of QS promoters in E. coli hns. The largest decrease in the level of H-NS repression was observed using ligands containing a linker with a length of ca. 18Å, such as DBP(2) and DBPA(2). Ligands containing linkers with n=1 and 3 are an order of magnitude less active; ligands with n=4 are inactive. DBPA(2) exhibits activity starting with a concentration of 0.5μM; the minimum concentration of DBP(2) is 5-7 times higher. It is suggested that A-T pairs located at five nucleotide pair intervals, which correspond to the linker length in highly active ligands with n=2, play a key role in the structure of H-NS-binding sites in QS-regulated promoters.

1151 related Products with: DNA sequence-specific dimeric bisbenzimidazoles DBP(n) and DBPA(n) as inhibitors of H-NS silencing in bacterial cells.

GLP 1 ELISA Kit, Rat Gluc removed without changing EnzyChrom™ Kinase Assay MarkerGeneTM in vivo lacZ MarkerGeneTM Live Dead As pCAMBIA0105.1R Vector, (G OxiSelect™ Cellular UV- HIV 2 gp36 envelope antig Anti C Reactive Protein A Anti AGO2 Human, Monoclon Anti AGO2 Mouse, Monoclon Anti AGO2 Human, Monoclon

Related Pathways

paperclip

#29458345   // Save this To Up

Genetic polymorphisms in bone morphogenetic protein receptor type IA gene predisposes individuals to ossification of the posterior longitudinal ligament of the cervical spine via the smad signaling pathway.

The present study investigated the molecular mechanisms underlying the 4A > C and -349C > T single nucleotide polymorphisms (SNPs) in bone morphogenetic protein receptor type IA (BMPR-IA) gene, which significantly associated with the occurrence and the extent of ossification of the posterior longitudinal ligament (OPLL) in the cervical spine.

2751 related Products with: Genetic polymorphisms in bone morphogenetic protein receptor type IA gene predisposes individuals to ossification of the posterior longitudinal ligament of the cervical spine via the smad signaling pathway.

Anti-BMPR1A(Bone morphoge FDA Standard Frozen Tissu FDA Standard Frozen Tissu FDA Standard Frozen Tissu FDA Standard Frozen Tissu Anti-BMPR1B(Bone morphoge Anti BMPR1B(Bone morphoge Anti-Bone Morphogenetic P Anti Bone Morphogenetic P Recombinant Human PKC the Recombinant Human PKC the Recombinant Human PKC the

Related Pathways

paperclip

#29456451   // Save this To Up

Human β-defensin-2 gene transduction of dental pulp cells: A model for pulp antimicrobial gene therapy.

The objective of this study was to determine whether cells from human pulp can be transduced to express the antimicrobial peptide--human β-defensin-2 (HBD-2). Primary human pulp cells and gingival fibroblasts from normal tissue, as well as two mouse cell lines (NIH 3T3 and AT-84) and a human cell line SCC-9 were transduced with a retroviral vector carrying HBD-2 cDNA. ELISA and Northern blot analyses were performed to detect HBD-2 expression by these transduced cells. Antimicrobail assays using recombinant HBD-2 were performed on two caries-associated bacteriaand. The results showed that transduced pulp cells secreted 62.4 ± 27.2 ng/3 days of HBD-2, which was comparable to that by NIH 3T3 (78.0 ± 14.1 ng/4 days), and higher than those by gingival fibroblasts (17.9 ± 7.9 ng/3 days), AT-84 (2.6 ± 1.0 ng/3 days), and SCC-9 (47.6 ± 9.9 ng/3 days). Northern blot analysis showed that the levels of HBD-2 mRNA expression correlated with their protein secretion levels. There was approximately 50% reduction of growth whenandwere exposed to HBD-2 at 1 µM. Pulp cells appear to be suitable for HBD-2 transduction using retroviral vectors, suggesting a potential for use in controlling pulpal infections.

1193 related Products with: Human β-defensin-2 gene transduction of dental pulp cells: A model for pulp antimicrobial gene therapy.

Rabbit Anti-IEX1 Differen Rabbit Anti-IEX1 Differen Growth Differentiation Fa Human Epstein-Barr Virus Mouse Anti-Human Defensin Alpha- Amylase Blocking P Anti PDX1 Polyclonal Anti PUMA bbc3 Blocking Peptid ALK peptide;Appearance Co Cathepsin K Blocking Pept Heme Oxygenase-2 Blocking ICAM-1 Blocking Peptide;A

Related Pathways