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Fanconi anemia (FA) is a genomic instability disorder, clinically characterized by congenital abnormalities, progressive bone marrow failure, and predisposition to malignancy. Cells derived from patients with FA display a marked sensitivity to DNA cross-linking agents, such as mitomycin C (MMC). This observation has led to the hypothesis that the proteins defective in FA are involved in the sensing or repair of interstrand cross-link lesions of the DNA. A nuclear complex consisting of a majority of the FA proteins plays a crucial role in this process and is required for the monoubiquitination of a downstream target, FANCD2. Two new FA genes, FANCB and FANCL, have recently been identified, and their discovery has allowed a more detailed study into the molecular architecture of the FA pathway. We demonstrate a direct interaction between FANCB and FANCL and that a complex of these proteins binds FANCA. The interaction between FANCA and FANCL is dependent on FANCB, FANCG, and FANCM, but independent of FANCC, FANCE, and FANCF. These findings provide a framework for the protein interactions that occur "upstream" in the FA pathway and suggest that besides the FA core complex different subcomplexes exist that may have specific functions other than the monoubiquitination of FANCD2. IntroductionMultiple pathways are required by the cell to deal with endogenous and exogenous damage to the DNA and to maintain the genome's integrity. The inactivation of these pathways leads to an unstable genome, which increases the risk of tumorigenesis. Many of the genes involved in DNA repair and genomic stability are mutated in cancer predisposition syndromes such as XPA-G (xeroderma pigmentosum), NBS1 (Nijmegen breakage syndrome), and ATM (ataxia telangiectasia). The function of the gene products that are defective in the Fanconi anemia (FA) pathway, which is speculated to act in DNA repair, remains elusive.FA is clinically characterized by congenital abnormalities, progressive bone marrow failure, and predisposition to malignancy, especially acute myeloid leukemia (AML) and squamous cell carcinoma (SCC). Cells derived from patients with FA are hypersensitive to DNA cross-linking agents, such as mitomycin C (MMC) and diexpoxybutane (DEB), which suggests that the FA pathway may be involved in the sensing and/or repair of interstrand cross-links. Cell fusion experiments have identified 12 different complementation groups, and 11 of their corresponding disease genes have been cloned : FANCA, FANCB, FANCC, FANCD1/ BRCA2, FANCD2, FANCE, FANCF, FANCG, FANCJ/BRIP1, FANCL, Many of the FA proteins interact in a nuclear complex, the assembly of which is required for the monoubiquitination of a downstream target, FANCD2. 15 This protein has been the subject of intense investigation in recent years, and several studies have revealed that the monoubiquitinated isoform of FANCD2 enters discrete nuclear foci where it colocalizes with multiple proteins involved in genomic stability including BRCA1, NBS1, and RAD51. [15][16][17] Furthermore, it has b...

The electron spin dynamics in (111)-oriented GaAs/AlGaAs quantum wells is studied by timeresolved photoluminescence spectroscopy. By applying an external field of 50 kV/cm a two-order of magnitude increase of the spin relaxation time can be observed reaching values larger than 30 ns; this is a consequence of the electric field tuning of the spin-orbit conduction band splitting which can almost vanish when the Rashba term compensates exactly the Dresselhaus one. The measurements under transverse magnetic field demonstrate that the electron spin relaxation time for the three space directions can be tuned simultaneously with the applied electric field.The control of the electron spins in semiconductors for potential use in transport devices or quantum information applications has attracted a great attention in recent years [1][2][3]. In 2D nanostructures made of III-V or II-VI semiconductors, the dominant loss of electron spin memory is related to the spin relaxation mechanism known under the name Dyakonov-Perel (DP) [4,5]. In these materials, the absence of inversion symmetry and the spin-orbit (SO) coupling are responsible for the lifting of degeneracy for spin | 1/2 and | −1/2 electrons states in the conduction band (CB). This splitting plays a crucial role for the spin manipulation and spin transport phenomena [6,7]. As it depends strongly on the crystal and nanostructure symmetry [8][9][10], it can be efficiently tailored as explained below. The SO splitting can be viewed as the result of the action on the electron spin of an effective magnetic field whose amplitude and direction depend on the wave vector k of the electron. The electronic spin will precess around this field with an effective, momentum dependent, Larmor vector Ω whose magnitude corresponds to the CB spin splitting. This effective magnetic field changes with time since the direction of electron momentum varies due to electron collisions. As a consequence, spin precession around this field in the intervals between collisions gives rise to spin relaxation. In the usual case of frequent collisions, the relaxation time of an electron spin oriented along the direction i can be written [4]:where Ω 2 ⊥ is the mean square precession vector in the plane perpendicular to the direction i (i=x, y, z) and τ * p the electron momentum relaxation time. This yields the loss of the electron spin memory in a few tens or hundreds of picoseconds [11,12]. As the driving force in the DP spin relaxation is the SO splitting, its reduction is expected to lead to an increase of the spin relaxation time [13,14]. In bulk zinc blende semiconductor, the Bulk Inversion Asymmetry (BIA) spin splitting, also called Dresselhaus term, is determined by [1,8]:where γ is the Dresselhaus coefficient and k = (k x , k y , k z ) the electron wavector. In a quantum well (QW) where the momentum component along the growth axis z is quantized, the vector Ω due to the BIA for the lowest electron sub-band writes:where k 2 z is the averaged squared wavevector along the growth direction and k the...