Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0016632 (Fox)
 1,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Human immunodeficiency virus type 1 (HIV-1) can establish a persistent and latent infection in CD4+ T lymphocytes (W. C. Greene, N. Engl. J. Med. 324:308-317, 1991; S. M. Schnittman, M. C. Psallidopoulos, H. C. Lane, L. Thompson, M. Baseler, F. Massari, C. H. Fox, N. P. Salzman, and A. S. Fauci, Science 245:305-308, 1989). Production of HIV-1 from latently infected cells requires host cell activation by T-cell mitogens (T. Folks, D. M. Powell, M. M. Lightfoote, S. Benn, M. A. Martin, and A. S. Fauci, Science 231:600-602, 1986; D. Zagury, J. Bernard, R. Leonard, R. Cheynier, M. Feldman, P. S. Sarin, and R. C. Gallo, Science 231:850-853, 1986). This activation is mediated by the host transcription factor NF-kappa B [G. Nabel and D. Baltimore, Nature (London) 326:711-717, 1987]. We report here that the HIV-1-encoded Nef protein inhibits the induction of NF-kappa B DNA-binding activity by T-cell mitogens. However, Nef does not affect the DNA-binding activity of other transcription factors implicated in HIV-1 regulation, including SP-1, USF, URS, and NF-AT. Additionally, Nef inhibits the induction of HIV-1- and interleukin 2-directed gene expression, and the effect on HIV-1 transcription depends on an intact NF-kappa B-binding site. These results indicate that defective recruitment of NF-kappa B may underlie Nef's negative transcriptional effects on the HIV-1 and interleukin 2 promoters. Further evidence suggests that Nef inhibits NF-kappa B induction by interfering with a signal derived from the T-cell receptor complex.
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PMID:Human immunodeficiency virus type 1 Nef protein inhibits NF-kappa B induction in human T cells. 152 59

In our preceding paper [Ratnam, M., Sargent, P. B., Sarin, V., Fox, J. L., Le Nguyen, D., Rivier, J., Criado, M., & Lindstrom, J. (1986) Biochemistry (preceding paper in this issue)], we presented results from peptide mapping studies of purified subunits of the Torpedo acetylcholine receptor which suggested that the sequence beta 429-441 is on the cytoplasmic surface of the receptor. Since this finding contradicts earlier theoretical models of the transmembrane structure of the receptor, which placed this sequence of the beta subunit on the extracellular surface, we investigated the location of the corresponding sequence (389-408) and adjacent sequences of the alpha subunit by a more direct approach. We synthesized peptides including the sequences alpha 330-346, alpha 349-364, alpha 360-378, alpha 379-385, and alpha 389-408 and shorter parts of these peptides. These peptides corresponded to a highly immunogenic region, and by using 125I-labeled peptides as antigens, we were able to detect in our library of monoclonal antibodies to alpha subunits between two and six which bound specifically to each of these peptides, except alpha 389-408. We obtained antibodies specific for alpha 389-408 both from antisera against the denatured alpha subunit and from antisera made against the peptide. These antibodies were specific to alpha 389-396. In binding assays, antibodies specific for all of these five peptides bound to receptor-rich membrane vesicles only after permeabilization of the vesicles to permit access of the antibodies to the cytoplasmic surface of the receptors, suggesting that the receptor sequences which bound these antibodies were located on the intracellular side of the membrane. Electron microscopy using colloidal gold to visualize the bound antibodies was used to conclusively demonstrate that all of these sequences are exposed on the cytoplasmic surface of the receptor. These results, along with our previous demonstration that the C-terminal 10 amino acids of each subunit are exposed on the cytoplasmic surface, show that the hydrophobic domain M4 (alpha 409-426), previously predicted from hydropathy profiles to be transmembranous, does not, in fact, cross the membrane. Further, these results show that the putative amphipathic transmembrane domain M5 (alpha 364-399) also does not cross the membrane. Our results thus indicate that the transmembrane topology of a membrane protein cannot be deduced strictly from the hydropathy profile of its primary amino acid sequence. We present a model for the transmembrane orientation of receptor subunit polypeptide chains which is consistent with current data.
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PMID:Transmembrane topography of nicotinic acetylcholine receptor: immunochemical tests contradict theoretical predictions based on hydrophobicity profiles. 371 69

From the time of diagnosis of a primary malignant brain tumour (PMBT) and throughout the illness trajectory, the patient and intimate partner face many psychosocial challenges ranging from fear and uncertainty to hope and loss (Fox & Lantz, 1998; Janda et al., 2007; Kvale, Murthy, Taylor, Lee, & Nabors, 2009). While many patients diagnosed with cancer may go on to live with cancer as a chronic illness, this may not be said of individuals diagnosed with a PMBT, in particular those diagnosed with a glioma, the most common form of brain tumour (Gupta & Sarin, 2002). Gliomas are associated with a short disease trajectory and multiple deficits (functional, cognitive and psychiatric). What makes the PMBT experience unique from other cancers is that the intimate partner must not only deal with the diagnosis of cancer in their spouse, but also the accompanying personality, functional and behavioural changes wrought by the disease, as well as grieve the loss of the person they once knew (Sherwood et al., 2004). These multi-dimensional deficits are thought to place the intimate partner, as caregiver, at greater risk for adverse psychosocial effects such as anxiety, depression and post traumatic stress (Goebel, von Harscher, & Mehdorn, 2011; Keir, Farland, Lipp, & Friedman, 2009). The following discussion will provide an overview of the extant literature on the experience of living with a PMBT from the intimate partner (spouse) perspective with a particular emphasis on how intimate partners cope. The intimate partner is considered to be the heterosexual or same-sex, married or common-law partner of the patient. Highlights from the psychotherapy practice of the author will be used to further strengthen the need for more research, education and enhanced practice to more effectively meet the unique needs of this under-researched and supported population.
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PMID:Primary malignant brain tumours, psychosocial distress and the intimate partner experience: what do we know? 2563 13