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    Phone: Fax: E-mail: ude. Here we show a role for Abi, the Abi-binding partner Nap1, and the Nap1-binding protein Sra1 in the regulation of cadherin-dependent adhesion. Notably, an active Dia1 C-terminal fragment that localizes to cell-cell junctions rescued the abnormal junctions induced by depletion of Abi or Nap1 in epithelial cells. The formation of adhesive contacts between cells is essential for tissue morphogenesis and homeostasis, processes that are critically dependent on adherens junctions Adherens junctions link the actin cytoskeleton of neighboring cells by the binding of cadherins on contacting cells Actin polymerization provides the driving force for the formation of adherens junctions Assembly of intercellular adhesions is driven by lamellipodial or filopodial membrane protrusions in adjacent cells 8 , 17 , 29 dependent on the activity of Rho family GTPases, Rac and Cdc42 9.

    Formins nucleate unbranched actin filaments 11 , 30 , and formin-1 has been implicated in the formation of linear actin cables that radiate from cadherin-containing puncta Active Rac binds to this complex by interaction with Sra1, which interacts with Nap1, and in turn Nap1 is linked to Wave by Abi proteins.

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    Abi1 and Abi2, which constitute the core of the Wave complex 15 , were originally cloned as binding partners and substrates for the Abl tyrosine kinases 5 , Abi1 and Abi2 localize to sites of dynamic actin polymerization 7 , 12 , 26 , 36 , and Abi1 is required for platelet-derived growth factor-induced membrane ruffling and lamellipodial protrusion 15 , We showed that both Abi1 and Abi2 are required for actin polymerization at the T-cell-B-cell contact site A role for Abi in actin-dependent processes is also supported by our finding that small interfering RNA siRNA -mediated knockdown of Abi1 and Abi2 impairs cell-cell junctions Here we show that the Abi proteins regulate the formation and stability of cell-cell junctions by interacting with the Diaphanous Dia -related formins.

    Our data reveal a role for Abi proteins in the regulation of distinct types of actin nucleation machines at intercellular junctions.

    Plasmids and siRNAs. Antibodies and reagents. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

    This article has been cited by other articles in PMC. Abstract DNA and other biomolecules are subjected to damaging chemical reactions during normal physiological processes and in states of pathophysiology caused by endogenous and exogenous mechanisms.

    In DNA, this damage affects both the nucleobases and 2-deoxyribose, with a host of damage products that reflect the local chemical pathology such as oxidative stress and inflammation. These damaged molecules represent a potential source of biomarkers for defining mechanisms of pathology, quantifying the risk of human disease and studying interindividual variations in cellular repair pathways.

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    Toward the goal of developing biomarkers, significant effort has been made to detect and quantify damage biomolecules in clinically accessible compartments such as blood and and urine. However, there has been little effort to define the biotransformational fate of damaged biomolecules as they move from the site of formation to excretion in clinically accessible compartments. This paper highlights examples of this important problem with DNA damage products.

    Introduction Endogenous processes of oxidative stress and inflammation cause DNA damage that is mechanistically linked to the pathophysiology of cancer and other human diseases [ 1 ]. The DNA damage is comprised of dozens of mutagenic and cytotoxic products [ 2 — 4 ] reflecting the full spectrum of chemical mechanisms, including oxidation, nitrosation, halogenation, and alkylation, as described in numerous published reviews [ 5 — 15 ].

    There has been significant interest in developing DNA damage products as biomarkers of disease risk given the strong association between DNA damage and disease pathology [ 12 , 14 , 16 — 22 ]. However, there has been little consideration given to the biological fate of DNA damage products, such as release from DNA as a result of instability, repair, and reaction with local nucleophiles, and the effect of this fate on the steady-state level of DNA lesions in cells and tissues.

    Further, the use of tissue-derived DNA for biomarker development poses the problem of accessibility and limits clinical studies, so researchers are exploring the presence of DNA damage products in other sampling compartments, such as urine e.

    These efforts have presumed that DNA repair or cell death leads to dissemination of DNA damage products in blood, with subsequent excretion of specific molecular forms predicted to arise from the various DNA repair or other enzymatic processes. However, one of the major drawbacks to the use of blood or urine as a sampling compartment for development of DNA damage products as biomarkers is the lack of mechanistic information about the fates of the damage products in terms of metabolism and distribution.

    While information about the metabolic fate and pharmacokinetics of drugs based on nucleobases has been well defined e.

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