An internet user wanting to share observed content is typically restricted to primitive techniques such as screenshots, web caches or share button-like solutions. These acclaimed proofs, however, are either trivial to falsify or require trust in centralized entities (e.g., search engine caches). This motivates the need for a seamless and standardized internet-wide non-repudiation mechanism, all...

Cells cope with replication-blocking lesions via translesion DNA synthesis (TLS). TLS is carried out by low-fidelity DNA polymerases that replicate across lesions, thereby preventing genome instability at the cost of increased point mutations. Here we perform a two-stage siRNA-based functional screen for mammalian TLS genes and identify 17 validated TLS genes. One of the genes, NPM1, is frequen...

This document describes extensions that may be used to add functionality to TLS. It provides both generic extension mechanisms for the TLS handshake client and server hellos, and specific extensions using these generic mechanisms. The extensions may be used by TLS clients and servers. The extensions are backwards compatible communication is possible between TLS 1.0 clients that support the exte...

This memo proposes a mechanism to upgrade HTTP/1.1 connections to use Transport Layer Security (TLS). Using an Upgrade: TLS/x.y request header would allow unsecured and secured traffic to share the same port (in this case, 80). A companion document describes the current practice of using a separate port for HTTP over TLS, .

DNA replication across blocking lesions occurs by translesion DNA synthesis (TLS), involving a multitude of mutagenic DNA polymerases that operate to protect the mammalian genome. Using a quantitative TLS assay, we identified three main classes of TLS in human cells: two rapid and error-free, and the third slow and error-prone. A single gene, REV3L, encoding the catalytic subunit of DNA polymer...

Tumor lysis syndrome (TLS) complicating non-hematologic malignancy is infrequent and spontaneous TLS is a very rare occurrence in patients with solid tumors. We report a case of spontaneous TLS in a patient with metastatic melanoma. Clinicians should have awareness of the possibility of spontaneous TLS in patients with solid tumors and should recognize the clinical presentation and laboratory t...

TLS (translocation in liposarcoma), an RNA-binding protein, was originally identified as a heterogeneous ribonuclear protein (hnRNP). Recently, we showed that TLS is localized in neuronal dendrites of mouse hippocampal neurons and is translocated to the spines, where local translation takes place, in an mGluR5 activation-dependent manner. However, the specific role of TLS has not been clarified...

The oncogenic TLS-ERG fusion protein is found in human myeloid leukemia and Ewing's sarcoma as a result of specific chromosomal translocation. To unveil the potential mechanism(s) underlying cellular transformation, we have investigated the effects of TLS-ERG on both gene transcription and RNA splicing. Here we show that the TLS protein forms complexes with RNA polymerase II (Pol II) and the se...

The TLS-CHOP oncoprotein, found in the majority of human myxoid liposarcomas, consists of a fusion between the transcription factor CHOP/GADD153 and the N terminus of an RNA-binding protein TLS/FUS. Clinical correlation and in vitro transformation assays indicate that the N terminus of TLS plays an important role in oncogenesis by TLS-CHOP. Until now, however, the only activity attributed to th...

FUS/TLS is a nucleic acid binding protein that, when mutated, can cause a subset of familial amyotrophic lateral sclerosis (fALS). Although FUS/TLS is normally located predominantly in the nucleus, the pathogenic mutant forms of FUS/TLS traffic to, and form inclusions in, the cytoplasm of affected spinal motor neurons or glia. Here we report a yeast model of human FUS/TLS expression that recapi...