Continued from Anti-6X His tag antibodies, today I will overview Anti-V5 tag Mouse Monoclonal Antibodies.The V5 tag is derived from a small epitope (Pk) found on the P and V proteins of the paramyxovirus of simian virus 5 (SV5). The V5 tag is generally used with all 14 amino acids (GKPIPNPLLGLDST), but it may also be used with a shorter 9-amino acid (IPNPLLGLD) sequence. V5 tag antibodies provide a dependable method for the detection and purification of tagged target proteins without a protein-specific antibody or probe. The V5 epitope tag is commonly engineered onto the N- or C- terminus of a protein of interest so that the tagged protein can be analyzed and visualized using immunochemical methods.
Abbkine offers a wide selection of such as AbFluor 350, 405, 488, 555, 594, 647, 680, Cy3, Cy5, FITC, agarose, magnetic beads and HRP conjugated anti-V5 tag Monoclonal antibodies for your choice.
[table id=19 /]
About Abbkine Scientific Co., Ltd.
Abbkine Scientific Co., Ltd. is a leading biotechnology company that focuses on developing and providing innovative, high quality assay kits, recombinant proteins, antibodies and other research tools to accelerate life science fundamental research, drug discovery, etc. Find more details, please visit the website at Abbkine.
Anti-Myc tag antibodies will be continued next time.
2018年8月7日星期二
Anti-V5 tag Monoclonal Antibodies from Abbkine
PTBP1-Mediated Alternative Splicing Regulates the Inflammatory Secretome and the Pro-tumorigenic Effects of Senescent Cells
Content introduction:
- PTBP1-Mediated Alternative Splicing Regulates the Inflammatory Secretome and the Pro-tumorigenic Effects of Senescent Cells
- The Tandem Duplicator Phenotype Is a Prevalent Genome-Wide Cancer Configuration Driven by Distinct Gene Mutations
- EZH2-Mediated Primary Cilium Deconstruction Drives Metastatic Melanoma Formation
- Apoptotic Cell-Derived Extracellular Vesicles Promote Malignancy of Glioblastoma Via Intercellular Transfer of Splicing Factors
- A Comprehensive Pan-Cancer Molecular Study of Gynecologic and Breast Cancers
1. PTBP1-Mediated Alternative Splicing Regulates the Inflammatory Secretome and the Pro-tumorigenic Effects of Senescent Cells
Oncogene-induced senescence is a potent tumor-suppressive response. Paradoxically, senescence also induces an inflammatory secretome that promotes carcinogenesis and age-related pathologies. Consequently, the senescence-associated secretory phenotype (SASP) is a potential therapeutic target. Here, Athena Georgilis at MRC London Institute of Medical Sciences (LMS) in London, UK and her colleagues describe an RNAi screen for SASP regulators. They identified 50 druggable targets whose knockdown suppresses the inflammatory secretome and differentially affects other SASP components. Among the screen candidates was PTBP1. PTBP1 regulates the alternative splicing of genes involved in intracellular trafficking, such as EXOC7, to control the SASP. Inhibition of PTBP1 prevents the pro-tumorigenic effects of the SASP and impairs immune surveillance without increasing the risk of tumorigenesis. In conclusion, their study identifies SASP inhibition as a powerful and safe therapy against inflammation-driven cancer.
Read more, please click https://www.cell.com/cancer-cell/fulltext/S1535-6108(18)30264-2
2. The Tandem Duplicator Phenotype Is a Prevalent Genome-Wide Cancer Configuration Driven by Distinct Gene Mutations
The tandem duplicator phenotype (TDP) is a genome-wide instability configuration primarily observed in breast, ovarian, and endometrial carcinomas. Here, Francesca Menghi at The Jackson Laboratory for Genomic Medicine in Farmington, USA and his colleagues stratify TDP tumors by classifying their tandem duplications (TDs) into three span intervals, with modal values of 11 kb, 231 kb, and 1.7 Mb, respectively. TDPs with ∼11 kb TDs feature loss of TP53 and BRCA1. TDPs with ∼231 kb and ∼1.7 Mb TDs associate with CCNE1 pathway activation and CDK12 disruptions, respectively. They demonstrate that p53 and BRCA1 conjoint abrogation drives TDP induction by generating short-span TDP mammary tumors in genetically modified mice lacking them. Lastly, they show how TDs in TDP tumors disrupt heterogeneous combinations of tumor suppressors and chromatin topologically associating domains while duplicating oncogenes and super-enhancers.
Read more, please click https://www.cell.com/cancer-cell/fulltext/S1535-6108(18)30265-4
3. EZH2-Mediated Primary Cilium Deconstruction Drives Metastatic Melanoma Formation
Human melanomas frequently harbor amplifications of EZH2. However, the contribution of EZH2 to melanoma formation has remained elusive. Taking advantage of murine melanoma models, Daniel Zingg at The Netherlands Cancer Institute in Amsterdam, the Netherlands and his colleagues show that EZH2 drives tumorigenesis from benign Braf V600E- or Nras Q61K-expressing melanocytes by silencing of genes relevant for the integrity of the primary cilium, a signaling organelle projecting from the surface of vertebrate cells. Consequently, gain of EZH2 promotes loss of primary cilia in benign melanocytic lesions. In contrast, blockade of EZH2 activity evokes ciliogenesis and cilia-dependent growth inhibition in malignant melanoma. Finally, they demonstrate that loss of cilia enhances pro-tumorigenic WNT/β-catenin signaling, and is itself sufficient to drive metastatic melanoma in benign cells. Thus, primary cilia deconstruction is a key process in EZH2-driven melanomagenesis.
Read more, please click https://www.cell.com/cancer-cell/fulltext/S1535-6108(18)30229-0
4. Apoptotic Cell-Derived Extracellular Vesicles Promote Malignancy of Glioblastoma Via Intercellular Transfer of Splicing Factors
Aggressive cancers such as glioblastoma (GBM) contain intermingled apoptotic cells adjacent to proliferating tumor cells. Nonetheless, intercellular signaling between apoptotic and surviving cancer cells remain elusive. In this study, Marat S. Pavlyukov at University of Alabama at Birmingham in Birmingham, USA and his colleagues demonstrate that apoptotic GBM cells paradoxically promote proliferation and therapy resistance of surviving tumor cells by secreting apoptotic extracellular vesicles (apoEVs) enriched with various components of spliceosomes. apoEVs alter RNA splicing in recipient cells, thereby promoting their therapy resistance and aggressive migratory phenotype. Mechanistically, they identified RBM11 as a representative splicing factor that is upregulated in tumors after therapy and shed in extracellular vesicles upon induction of apoptosis. Once internalized in recipient cells, exogenous RBM11 switches splicing of MDM4 and Cyclin D1 toward the expression of more oncogenic isoforms.
Read more, please click https://www.cell.com/cancer-cell/fulltext/S1535-6108(18)30226-5
5. A Comprehensive Pan-Cancer Molecular Study of Gynecologic and Breast Cancers
Ashton C. Berger at The Eli and Edythe L. Broad Institute of Massachusetts Institute of Technology and Harvard University in Cambridge, USA and his colleagues analyzed molecular data on 2,579 tumors from The Cancer Genome Atlas (TCGA) of four gynecological types plus breast. Their aims were to identify shared and unique molecular features, clinically significant subtypes, and potential therapeutic targets. They found 61 somatic copy-number alterations (SCNAs) and 46 significantly mutated genes (SMGs). Eleven SCNAs and 11 SMGs had not been identified in previous TCGA studies of the individual tumor types. They found functionally significant estrogen receptor-regulated long non-coding RNAs (lncRNAs) and gene/lncRNA interaction networks. Pathway analysis identified subtypes with high leukocyte infiltration, raising potential implications for immunotherapy. Using 16 key molecular features, they identified five prognostic subtypes and developed a decision tree that classified patients into the subtypes based on just six features that are assessable in clinical laboratories.
Read more, please click https://www.cell.com/cancer-cell/fulltext/S1535-6108(18)30119-3
2018年8月6日星期一
The Nobel Prize in Physiology or Medicine 2010
The Nobel Prize in Physiology or Medicine 2010 was awarded to Robert G. Edwards "for the development of in vitro fertilization".
Robert G. Edwards
Born: 27 September 1925, Batley, United Kingdom
Died: 10 April 2013, Cambridge, United Kingdom
Affiliation at the time of the award: University of Cambridge, Cambridge, United Kingdom
Summary
Robert Edwards is awarded the 2010 Nobel Prize for the development of human in vitro fertilization (IVF) therapy. His achievements have made it possible to treat infertility, a medical condition afflicting a large proportion of humanity including more than 10% of all couples worldwide.
As early as the 1950s, Edwards had the vision that IVF could be useful as a treatment for infertility. He worked systematically to realize his goal, discovered important principles for human fertilization, and succeeded in accomplishing fertilization of human egg cells in test tubes (or more precisely, cell culture dishes). His efforts were finally crowned by success on 25 July, 1978, when the world's first "test tube baby" was born. During the following years, Edwards and his co-workers refined IVF technology and shared it with colleagues around the world.
Approximately four million individuals have so far been born following IVF. Many of them are now adult and some have already become parents. A new field of medicine has emerged, with Robert Edwards leading the process all the way from the fundamental discoveries to the current, successful IVF therapy. His contributions represent a milestone in the development of modern medicine.
More details, please click The 2010 Nobel Prize in Physiology or Medicine.
2018年8月5日星期日
The Nobel Prize in Physiology or Medicine 2010
The Nobel Prize in Physiology or Medicine 2010 was awarded to Robert G. Edwards "for the development of in vitro fertilization".
Robert G. Edwards
Born: 27 September 1925, Batley, United Kingdom
Died: 10 April 2013, Cambridge, United Kingdom
Affiliation at the time of the award: University of Cambridge, Cambridge, United Kingdom
Summary
Robert Edwards is awarded the 2010 Nobel Prize for the development of human in vitro fertilization (IVF) therapy. His achievements have made it possible to treat infertility, a medical condition afflicting a large proportion of humanity including more than 10% of all couples worldwide.
As early as the 1950s, Edwards had the vision that IVF could be useful as a treatment for infertility. He worked systematically to realize his goal, discovered important principles for human fertilization, and succeeded in accomplishing fertilization of human egg cells in test tubes (or more precisely, cell culture dishes). His efforts were finally crowned by success on 25 July, 1978, when the world's first "test tube baby" was born. During the following years, Edwards and his co-workers refined IVF technology and shared it with colleagues around the world.
Approximately four million individuals have so far been born following IVF. Many of them are now adult and some have already become parents. A new field of medicine has emerged, with Robert Edwards leading the process all the way from the fundamental discoveries to the current, successful IVF therapy. His contributions represent a milestone in the development of modern medicine.
More details, please click The 2010 Nobel Prize in Physiology or Medicine.
Anti-6X His tag antibodies from Abbkine
Abbkine provides anti-6X His tag Monoclonal and Polyclonal antibodies which are validated for use in applications such as western blot, Immunofluorescence and Immunoprecipitation. Also offers AbFluor 350, 405, 488, 555, 594, 647, 680, Cy3, Cy5, FITC, agarose, magnetic beads and HRP conjugated anti-His tag antibodies to meet all your research needs.
You can always find a product that best suits your experiment below.
[table id=18 /]
About Abbkine Scientific Co., Ltd.
Abbkine Scientific Co., Ltd. is a leading biotechnology company that focuses on developing and providing innovative, high quality assay kits, recombinant proteins, antibodies and other research tools to accelerate life science fundamental research, drug discovery, etc. Find more details, please visit the website at Abbkine.
Anti-V5 tag antibodies will be continued next time.
Anti-6X His tag antibodies from Abbkine
Abbkine provides anti-6X His tag Monoclonal and Polyclonal antibodies which are validated for use in applications such as western blot, Immunofluorescence and Immunoprecipitation. Also offers AbFluor 350, 405, 488, 555, 594, 647, 680, Cy3, Cy5, FITC, agarose, magnetic beads and HRP conjugated anti-His tag antibodies to meet all your research needs.
You can always find a product that best suits your experiment below.
[table id=18 /]
About Abbkine Scientific Co., Ltd.
Abbkine Scientific Co., Ltd. is a leading biotechnology company that focuses on developing and providing innovative, high quality assay kits, recombinant proteins, antibodies and other research tools to accelerate life science fundamental research, drug discovery, etc. Find more details, please visit the website at Abbkine.
Anti-V5 tag antibodies will be continued next time.
Anti-6X His tag antibodies from Abbkine
Abbkine provides anti-6X His tag Monoclonal and Polyclonal antibodies which are validated for use in applications such as western blot, Immunofluorescence and Immunoprecipitation. Also offers AbFluor 350, 405, 488, 555, 594, 647, 680, Cy3, Cy5, FITC, agarose, magnetic beads and HRP conjugated anti-His tag antibodies to meet all your research needs.
You can always find a product that best suits your experiment below.
[table id=18 /]
About Abbkine Scientific Co., Ltd.
Abbkine Scientific Co., Ltd. is a leading biotechnology company that focuses on developing and providing innovative, high quality assay kits, recombinant proteins, antibodies and other research tools to accelerate life science fundamental research, drug discovery, etc. Find more details, please visit the website at Abbkine.
Anti-V5 tag antibodies will be continued next time.
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