Five-branes in M(atrix) Theory

We propose a construction of five-branes which fill both light-cone dimensions in Banks, Fischler, Shenker and Susskind's matrix model of M theory. We argue that they have the correct long-range fields and spectrum of excitations. We prove Dirac charge quantization with the membrane by showing that the five-brane induces a Berry phase in the membrane world-volume theory, with a familiar magnetic monopole form.Comment: harvmac, 10 p

The Octonionic Membrane

We generalize the supermembrane solution of D=11 supergravity by permitting the 4-form $G$ to be either self-dual or anti-self-dual in the eight dimensions transverse to the membrane. After analyzing the supergravity field equations directly, and also discussing necessary conditions for unbroken supersymmetry, we focus on two specific, related solutions. The self-dual solution is not asymptotically flat. The anti-self-dual solution is asymptotically flat, has finite mass per unit area and saturates the same mass=charge Bogomolnyi bound as the usual supermembrane. Nevertheless, neither solution preserves any supersymmetry. Both solutions involve the octonionic structure constants but, perhaps surprisingly, they are unrelated to the octonionic instanton 2-form $F$, for which $TrF \wedge F$ is neither self-dual nor anti-self-dual.Comment: 17 pages, Latex; enhanced discussion on supersymmetry, some references adde

Spectrum of Eleven-dimensional Supergravity on a PP-wave Background

We calculate the spectrum of the linearized supergravity around the maximally supersymmetric pp-wave background in eleven dimensions. The resulting spectrum agrees with that of zero-mode Hamiltonian of a supermembrane theory on the pp-wave background. We also discuss the connection with the Kaluza-Klein zero modes of AdS_4 x S^7 background.Comment: 17 pages, no figures, LaTeX2e, typos correcte

ΔNp63 transcriptionally regulates ATM to control p53 Serine-15 phosphorylation

Background: Delta Np63 alpha is an epithelial progenitor cell marker that maintains epidermal stem cell self-renewal capacity. Previous studies revealed that UV-damage induced p53 phosphorylation is confined to Delta Np63 alpha-positive cells in the basal layer of human epithelium. Results: We now report that phosphorylation of the p53 tumour suppressor is positively regulated by Delta Np63 alpha in immortalised human keratinocytes. Delta Np63 alpha depletion by RNAi reduces steady-state ATM mRNA and protein levels, and attenuates p53 Serine-15 phosphorylation. Conversely, ectopic expression of Delta Np63 alpha in p63-null tumour cells stimulates ATM transcription and p53 Serine-15 phosphorylation. We show that ATM is a direct Delta Np63 alpha transcriptional target and that the Delta Np63 alpha response element localizes to the ATM promoter CCAAT sequence. Structure-function analysis revealed that the Delta Np63-specific TA2 transactivation domain mediates ATM transcription in coordination with the DNA binding and SAM domains. Conclusions: Germline p63 point mutations are associated with a range of ectodermal developmental disorders, and targeted p63 deletion in the skin causes premature ageing. The Delta Np63 alpha-ATM-p53 damage-response pathway may therefore function in epithelial development, carcinogenesis and the ageing processes

p-p' Branes in PP-wave Background

We present several supergravity solutions corresponding to both Dp, as well as Dp-Dp' systems, in NS-NS and R-R PP-wave background originating from AdS_3 times S^3 times R^4. The Dp brane solutions, p=1,..,5 are fully localized, whereas Dp-Dp' are localized along common transverse directions. We also discuss the supersymmetry properties of these solutions and the worldsheet construction for the p-p' system.Comment: 17 pages, v5: supergrav. solns. corrected, v6: more results added: now includes p-p' branes in both NS-NS and R-R PP-wave background, some restructuring of the tex

Spinorial geometry and Killing spinor equations of 6-D supergravity

We solve the Killing spinor equations of 6-dimensional (1,0)-supergravity coupled to any number of tensor, vector and scalar multiplets in all cases. The isotropy groups of Killing spinors are Sp(1)\cdot Sp(1)\ltimes \bH (1), U(1)\cdot Sp(1)\ltimes \bH (2), Sp(1)\ltimes \bH (3,4), $Sp(1) (2)$, $U(1) (4)$ and $\{1\} (8)$, where in parenthesis is the number of supersymmetries preserved in each case. If the isotropy group is non-compact, the spacetime admits a parallel null 1-form with respect to a connection with torsion the 3-form field strength of the gravitational multiplet. The associated vector field is Killing and the 3-form is determined in terms of the geometry of spacetime. The Sp(1)\ltimes \bH case admits a descendant solution preserving 3 out of 4 supersymmetries due to the hyperini Killing spinor equation. If the isotropy group is compact, the spacetime admits a natural frame constructed from 1-form spinor bi-linears. In the $Sp(1)$ and U(1) cases, the spacetime admits 3 and 4 parallel 1-forms with respect to the connection with torsion, respectively. The associated vector fields are Killing and under some additional restrictions the spacetime is a principal bundle with fibre a Lorentzian Lie group. The conditions imposed by the Killing spinor equations on all other fields are also determined.Comment: 34 pages, Minor change

Senataxin, defective in ataxia oculomotor apraxia type 2, is involved in the defense against oxidative DNA damage.

A defective response to DNA damage is observed in several human autosomal recessive ataxias with oculomotor apraxia, including ataxia-telangiectasia. We report that senataxin, defective in ataxia oculomotor apraxia (AOA) type 2, is a nuclear protein involved in the DNA damage response. AOA2 cells are sensitive to H2O2, camptothecin, and mitomycin C, but not to ionizing radiation, and sensitivity was rescued with full-length SETX cDNA. AOA2 cells exhibited constitutive oxidative DNA damage and enhanced chromosomal instability in response to H2O2. Rejoining of H2O2-induced DNA double-strand breaks (DSBs) was significantly reduced in AOA2 cells compared to controls, and there was no evidence for a defect in DNA single-strand break repair. This defect in DSB repair was corrected by full-length SETX cDNA. These results provide evidence that an additional member of the autosomal recessive AOA is also characterized by a defective response to DNA damage, which may contribute to the neurodegeneration seen in this syndrome