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Biomedical subjects

E A Riley

Publications and source records attributed to E A Riley.

8 recordsLinked to original sources
PubMed1999

The residues between the two transformation effector sites of Epstein-Barr virus latent membrane protein 1 are not critical for B-lymphocyte growth transformation.

Epstein-Barr virus (EBV) latent membrane protein 1 (LMP1) is essential for EBV-mediated transformation of primary B lymphocytes. LMP1 spontaneously aggregates in the plasma membrane and enables two transformation effector sites (TES1 and TES2) within the 200-amino-acid cytoplasmic carboxyl terminus to constitutively engage the tumor necrosis factor receptor (TNFR)-associated factors TRAF1, TRAF2, TRAF3, and TRAF5 and the TNFR-associated death domain proteins TRADD and RIP, thereby activating NF-kappaB and c-Jun N-terminal kinase (JNK). To investigate the importance of the 60% of the LMP1 carboxyl terminus that lies between the TES1-TRAF and TES2-TRADD and -RIP binding sites, an EBV recombinant was made that contains a specific deletion of LMP1 codons 232 to 351. Surprisingly, the deletion mutant was similar to wild-type (wt) LMP1 EBV recombinants in its efficiency in transforming primary B lymphocytes into lymphoblastoid cell lines (LCLs). Mutant and wt EBV-transformed LCLs were similarly efficient in long-term outgrowth and in regrowth after endpoint dilution. Mutant and wt LMP1 proteins were also similar in their constitutive association with TRAF1, TRAF2, TRAF3, TRADD, and RIP. Mutant and wt EBV-transformed LCLs were similar in steady-state levels of Bcl2, JNK, and activated JNK proteins. The wt phenotype of recombinants with LMP1 codons 232 to 351 deleted further demarcates TES1 and TES2, underscores their central importance in B-lymphocyte growth transformation, and provides a new perspective on LMP1 sequence variation between TES1 and TES2.

B-Lymphocytes↗
PubMed1999

The Epstein-Barr virus oncoprotein latent membrane protein 1 engages the tumor necrosis factor receptor-associated proteins TRADD and receptor-interacting protein (RIP) but does not induce apoptosis or require RIP for NF-kappaB activation.

A site in the Epstein-Barr virus (EBV) transforming protein LMP1 that constitutively associates with the tumor necrosis factor receptor 1 (TNFR1)-associated death domain protein TRADD to mediate NF-kappaB and c-Jun N-terminal kinase activation is critical for long-term lymphoblastoid cell proliferation. We now find that LMP1 signaling through TRADD differs from TNFR1 signaling through TRADD. LMP1 needs only 11 amino acids to activate NF-kappaB or synergize with TRADD in NF-kappaB activation, while TNFR1 requires approximately 70 residues. Further, LMP1 does not require TRADD residues 294 to 312 for NF-kappaB activation, while TNFR1 requires TRADD residues 296 to 302. LMP1 is partially blocked for NF-kappaB activation by a TRADD mutant consisting of residues 122 to 293. Unlike TNFR1, LMP1 can interact directly with receptor-interacting protein (RIP) and stably associates with RIP in EBV-transformed lymphoblastoid cell lines. Surprisingly, LMP1 does not require RIP for NF-kappaB activation. Despite constitutive association with TRADD or RIP, LMP1 does not induce apoptosis in EBV-negative Burkitt lymphoma or human embryonic kidney 293 cells. These results add a different perspective to the molecular interactions through which LMP1, TRADD, and RIP participate in B-lymphocyte activation and growth.

Antigens, CD↗
PubMed1991

Eating disorders as addictive behavior. Integrating 12-step programs into treatment planning.

To be effective in treating eating-disordered individuals, we must be open to working with an electric model of treatment. Often health care providers have difficulty with the addiction model of treatment, even though many eating-disordered patients will attest to the assistance and support they receive from these programs. It will be useful for both health care professionals and 12-step programs to avoid taking competitive positions. It is far more useful for professionals to have a working knowledge of how these programs work and how they can be of use to the individuals with eating disorders. Knowledge of local resources will also be of great value. Given the assistance that the clients tell us they receive at these programs, it makes more sense to understand and use these programs more, not less. There is evidence that eating disorder behaviors are addictive behavior, both from a psychological and physiologic perspective. Use of a 12-step program will assist with the practical details of helping individuals to stop employing self-destructive behaviors as well as provide support and decrease feelings of isolation and depression. It is important to integrate the 12-step program components into an overall treatment program to make the best use of both programs and decrease the competition usually inherent in both programs.

Behavior Therapy↗
PubMed1991

Codependency and the eating-disorder client.

The treatment of eating-disordered individuals with codependency is difficult. This article reviews the causes of eating disorders and codependency and cites similarities between these disorders. The recovery process and treatment needs of this population are explored. Psychotherapy, which is the treatment of choice, is reviewed in detail.

Adaptation, Psychological↗
PubMed1990

Bone marrow stromal cells modulate both kappa light chain and Ly1 antigen expression on Ly1+ pre-B cell lines in vitro.

Murine Ly1+ pre-B cell lines, including 70Z/3 and three pre-B cell lines derived from long-term bone marrow cultures, exhibited selective adherence to bone marrow stromal cells. In contrast, splenic B cells, the A20 B-cell lymphoma, and four Ly1- B cell lines derived from long-term bone marrow cultures failed to adhere substiantially to bone marrow cultures failed to adhere substiantially to bone marrow stroma. Ly1+ pre-B cell lines were induced to express kappa light chains by exposure to either lipopolysaccharide (LPS), recombinant interleukin-1 (IL-1), or stromal cells. However, induction of kappa light chains failed to prevent pre-B cell adherence to stromal cells. Supernatants derived from primary bone marrow stromal cells decreased Ly1 expression on the Ly1+ pre-B cell lines. These experiments suggest that (1) expression of immunoglobulin light chains by developing Ly1+ pre-B cells is mediated by bone marrow stromal cells; (2) loss of specific adherence to stroma is progressive and occurs post-light chain induction; and (3) soluble products of stromal cells may downregulate expression of surface Ly1 on otherwise Ly1+ pre-B cells. The importance of these observations to the development of both the Ly1- and Ly1+ B cell lineages in the mouse is discussed.

Animals↗
PubMed1989

Abnormal development of B cells and B cell progenitors in autoimmune (NZB x NZW)F1 mice.

The (NZB x NZW)F1 (BWF1) autoimmune strain displays reduced numbers of both c mu+ pre-B cells and Ly5(220)+ B cell progenitors in the bone marrow. The loss of these B cell precursor populations in the bone marrow increases with age. In contrast, the bone marrow of BWF1 mice possesses sIg+ B cells comparable in both number and surface phenotype to that observed in conventional strains. Analysis of the surface densities of both sIg and Ly5(220) antigens indicates that BWF1 bone marrow B cells comprise a heterogeneous population of both immature and mature B cells. In addition, BWF1 bone marrow still possessed progenitor cells capable of yielding newly generated B cell precursors and B cells in vitro. The diminished levels of intermediate B cell progenitors observed in BWF1 bone marrow may reflect abnormal regulation of B lineage differentiation during the life span of this autoimmune strain.

Animals↗