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News Article | December 6, 2016
Site: www.marketwired.com

SEATTLE, WA--(Marketwired - Dec 6, 2016) - Ranjit Mulgaonkar, President and COO of Zahalo, formerly DNA Response, has joined the board of the Electronic Retailing Association (ERA), which includes other members from companies such as QVC, HSN, Telebrands and Guthy-Renker. "I've been involved with ERA for about 5 years now having participated in various committees and speaking engagements and I have also written some content for the blog. With the board appointment, I know I will be able to contribute even more value that will help marketers tackle the changing e-commerce environment," said Mulgaonkar. "I am honored to be on the board and am looking forward to working with other industry leaders to educate ERA members and help grow the organization." As a member of the board, Mulgaonkar will bring extensive knowledge related to e-commerce that will help ERA members understand the challenges and benefits of digital marketing. His previous experience as the founder of DNA Response and before that, as an executive at Amazon, will provide ERA members with the guidance needed to adapt to a rapidly evolving digital marketing industry. "We at the ERA are elated to have Ranjit join our Board of Directors. He brings a wealth of knowledge on the digital side of the house that will very much complement our new board slate. We are thrilled to welcome him aboard," said Chris Reinmuth, President and CEO of the Electronic Retailing Association. To learn more about Ranjit Mulgaonkar, visit him on LinkedIn at https://www.linkedin.com/in/RanjitM. The Electronic Retailing Association (ERA) serves as the exclusive trade association representing the $350 billion direct-to-consumer marketplace. ERA membership spans the globe to encompass all levels of direct marketers, from start-up companies to global leaders that employ the power of direct response to market across all platforms including television, digital media and radio to achieve a consumer-direct, measurable and accountable response. In addition to helping grow its members' business opportunities and profitability as a major resource for networking, business tools and information, ERA is also the voice of the direct-to-consumer industry in the nation's Capital, working daily to protect the regulatory and legislative climate in an ongoing effort to ensure direct response marketers' ability to bring quality products and services to the consumer. Through its acclaimed self-regulatory guidelines, ERA is also dedicated to building consumer trust in direct response-marketed products and services. For more information, Retailing.org. Zahalo believes that trust is the key to growth and long-term performance for consumer product brands. They develop best-in-class services in digital marketing, web development, marketplaces management, distributed ecommerce, and analytics. Zahalo was founded in 2016 from a merger between Bluewater Digital and DNA Response with offices in Seattle, Washington; Clearwater, Florida; Philadelphia, Pennsylvania; and Pune, India. Learn more at Zahalo.com.


Ward J.D.,DNA Response | Muzzini D.M.,University of Milan | Petalcorin M.I.R.,DNA Response | Martinez-Perez E.,Imperial College London | And 5 more authors.
Molecular Cell | Year: 2010

Homologous recombination (HR) is essential for repair of meiotic DNA double-strand breaks (DSBs). Although the mechanisms of RAD-51-DNA filament assembly and strand exchange are well characterized, the subsequent steps of HR are less well defined. Here, we describe a synthetic lethal interaction between the C. elegans helicase helq-1 and RAD-51 paralog rfs-1, which results in a block to meiotic DSB repair after strand invasion. Whereas RAD-51-ssDNA filaments assemble at meiotic DSBs with normal kinetics in helq-1, rfs-1 double mutants, persistence of RAD-51 foci and genetic interactions with rtel-1 suggest a failure to disassemble RAD-51 from strand invasion intermediates. Indeed, purified HELQ-1 and RFS-1 independently bind to and promote the disassembly of RAD-51 from double-stranded, but not single-stranded, DNA filaments via distinct mechanisms in vitro. These results indicate that two compensating activities are required to promote postsynaptic RAD-51 filament disassembly, which are collectively essential for completion of meiotic DSB repair. © 2010 Elsevier Inc. All rights reserved.


Adamo A.,CNR Institute of Neuroscience | Collis S.J.,DNA Response | Collis S.J.,University of Sheffield | Adelman C.A.,DNA Response | And 8 more authors.
Molecular Cell | Year: 2010

Fanconi anemia (FA) is a complex cancer susceptibility disorder associated with DNA repair defects and infertility, yet the precise function of the FA proteins in genome maintenance remains unclear. Here we report that C. elegans FANCD2 (fcd-2) is dispensable for normal meiotic recombination but is required in crossover defective mutants to prevent illegitimate repair of meiotic breaks by nonhomologous end joining (NHEJ). In mitotic cells, we show that DNA repair defects of C. elegans fcd-2 mutants and FA-deficient human cells are significantly suppressed by eliminating NHEJ. Moreover, NHEJ factors are inappropriately recruited to sites of replication stress in the absence of FANCD2. Our findings are consistent with the interpretation that FA results from the promiscuous action of NHEJ during DNA repair. We propose that a critical function of the FA pathway is to channel lesions into accurate, as opposed to error-prone, repair pathways. © 2010 Elsevier Inc.


Horejsi Z.,DNA Response | Takai H.,Rockefeller University | Adelman C.A.,DNA Response | Collis S.J.,DNA Response | And 6 more authors.
Molecular Cell | Year: 2010

TEL2 interacts with and is essential for the stability of all phosphatidylinositol 3-kinase-related kinases (PIKKs), but its mechanism of action remains unclear. Here, we show that TEL2 is constitutively phosphorylated on conserved serines 487 and 491 by casein kinase 2 (CK2). Proteomic analyses establish that the CK2 phosphosite of TEL2 confers binding to the R2TP/prefoldin-like complex, which possesses chaperon/prefoldin activities required during protein complex assembly. The PIH1D1 subunit of the R2TP complex binds directly to the CK2 phosphosite of TEL2 in vitro and is required for the TEL2-R2TP/prefoldin-like complex interaction in vivo. Although the CK2 phosphosite mutant of TEL2 retains association with the PIKKs and HSP90 in cells, failure to interact with the R2TP/prefoldin-like complex results in instability of the PIKKs, principally mTOR and SMG1. We propose that TEL2 acts as a scaffold to coordinate the activities of R2TP/prefoldin-like and HSP90 chaperone complexes during the assembly of the PIKKs. © 2010 Elsevier Inc.


Prendergast A.M.,DNA Response | Cruet-Hennequart S.,DNA Response | Shaw G.,National University of Ireland | Barry F.P.,National University of Ireland | Carty M.P.,DNA Response
Cell Cycle | Year: 2011

DNA damaging agents are widely used in treatment of hematogical malignancies and solid tumors. While effects on hematopoietic stem cells have been characterized, less is known about the DNA damage response in human mesenchymal stem cells (hMSCs) in the bone marrow stroma, progenitors of osteoblasts, chondrocytes and adipocytes. To elucidate the response of undifferentiated hMSCs to γ-irradiation and cisplatin, key DNA damage responses have been characterized in hMSCs from normal adult donors. Cisplatin and γ-irradiation activated the DNA damage response in hMSCs, including induction of p53 and p21, and activation of PI3 kinase-related protein kinase (PIKK)-dependent phosphorylation of histone H2AX on serine 139, and replication protein A2 on serine4/serine8. Chemical inhibition of ATM or DNA-PK reduced DNA damage-induced phosphorylation of H2AX, indicating a role for both PIKKs in the response of hMSCs to DNA damage. Consistent with repair of DNA strand breaks, γH2AX staining decreased by 24 h following γ-irradiation. γ-irradiation arrested hMSCs in the G 1 phase of the cell cycle, while cisplatin induced S-phase arrest, mediated in part by the ATR /Chk1 checkpoint pathway. In hMSCs isolated from a chronic lymphocytic leukemia (CLL) patient, p53 and p21 were induced by cisplatin and γ-irradiation, while RPA2 was phosphorylated on serine4/8 in particular following cisplatin. Compared with peripheral blood lymphocytes or the leukemia cell line K562, both normal hMSCs and CLL-derived hMSCs were more resistant to cisplatin and γ-irradiation. These results provide insights into key pathways mediating the response of bone marrow-derived hMSCs to DNA damaging agents used in cancer treatment. © 2011 Landes Bioscience.


Zhao H.,DNA Response
Cell cycle (Georgetown, Tex.) | Year: 2014

Timely and proper cellular response to DNA damage is essential for maintenance of genome stability and integrity. B-cell lymphoma/leukemia 10 (BCL10) facilitates ubiquitination of NEMO in the cytosol, activating NFκB signaling. Translocation and/or point mutations of BCL10 associate with mucosa-associated lymphoid tissue lymphomas and other malignancies. However, the mechanisms by which the resulting aberrant expression of BCL10 leads to cellular oncogenesis are poorly understood. In this report, we found that BCL10 in the nucleus is enriched at the DNA damage sites in an ATM- and RNF8-dependent manner. ATM-dependent phosphorylation of BCL10 promotes its interaction with and presentation of UBC13 to RNF8, and RNF8-mediated ubiquitination of BCL10 enhances binding of BCL10 and UBC13 to RNF168. This allows mono-ubiquitination on H2AX by RNF168 and further poly-ubiquitination by the RNF8/RNF168-containing complex. Depletion of BCL10 compromised homology recombination-mediated DNA double-strand break (DSB) repair because of insufficient recruitment of BRCA1, RAD51, and the ubiquitinated DNA damage response factors. Taken together, our results demonstrate a novel function of BCL10 in delivering UBC13 to RNF8/RNF168 to regulate ubiquitination-mediated DSB signaling and repair.


Vannier J.-B.,DNA Response | Pavicic-Kaltenbrunner V.,DNA Response | Petalcorin M.I.R.,DNA Response | Ding H.,University of Manitoba | Boulton S.J.,DNA Response
Cell | Year: 2012

T loops and telomeric G-quadruplex (G4) DNA structures pose a potential threat to genome stability and must be dismantled to permit efficient telomere replication. Here we implicate the helicase RTEL1 in the removal of telomeric DNA secondary structures, which is essential for preventing telomere fragility and loss. In the absence of RTEL1, T loops are inappropriately resolved by the SLX4 nuclease complex, resulting in loss of the telomere as a circle. Depleting SLX4 or blocking DNA replication abolished telomere circles (TCs) and rescued telomere loss in RTEL1-/- cells but failed to suppress telomere fragility. Conversely, stabilization of telomeric G4-DNA or loss of BLM dramatically enhanced telomere fragility in RTEL1-deficient cells but had no impact on TC formation or telomere loss. We propose that RTEL1 performs two distinct functions at telomeres: it disassembles T loops and also counteracts telomeric G4-DNA structures, which together ensure the dynamics and stability of the telomere. © 2012 Elsevier Inc.


Online communications are susceptible to high levels of fraud or other unauthorized communications. Online sources of information about goods, including business-to-business resources, marketplace web sites, custom retail web sites, and the like may knowingly or unknowingly transmit communications representing counterfeit goods as genuine, communications regarding overstock goods at low prices without production and commission costs, and solicit customers anonymously. In some embodiments of the present disclosure, electronic information sources are monitored using data metrics to track electronic retailer activities, monitor distribution volumes by source, and monitor pricing. Analysis of such communications may be used to detect potentially fraudulent activity, and, based on manufacturer policy and threshold settings, may automatically report, notify, or take action against such illicit communications.


Online commercial activities are susceptible to high levels of fraud. Online sources of goods, including business-to-business resources, marketplace web sites, custom retail web sites, and the like may knowingly or unknowingly pass off counterfeit goods as genuine, sell overstock goods at low prices without production and commission costs, and solicit customers anonymously. In some embodiments of the present disclosure, electronic commerce sites are monitored using data metrics to track electronic retailer activities, monitor distribution volumes by source, and monitor pricing. Analysis of such items may be used to detect potentially fraudulent activity, and, based on manufacturer policy and threshold settings, may automatically report, notify, or take action against such illicit product sources.


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