Differential regulation of membrane and secretory mu chain synthesis in human beta cell lines. Regulation of membrane mu or secreted mu.

Hendershot, Linda M.; Levitt, Daniel

doi:10.1084/jem.156.6.1622

Cited by 15 publications

(6 citation statements)

References 42 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…However, in striking contrast, FCRLA antibodies ex-clusively immunoprecipitate the ls isoform (lower band). The assignment of these bands as lm and ls is based on differences in their SDS-PAGE mobility and is consistent with previous studies (33)(34)(35)(36).…”

Section: Fcrla Associates With Intracellular Igsupporting

confidence: 91%

FCRLA is a resident endoplasmic reticulum protein that associates with intracellular Igs, IgM, IgG and IgA

Santiago

Kulemzin

Reshetnikova

et al. 2010

International Immunology

View full text Add to dashboard Cite

Fc receptor-like A (FCRLA) is an unusual member of the extended Fc receptor family. FCRLA has homology to receptors for the Fc portion of Ig (FCR) and to other FCRL proteins. However, unlike these other family representatives, which are typically transmembrane receptors with extracellular ligand-binding domains, FCRLA has no predicted transmembrane domain or N-linked glycosylation sites and is an intracellular protein. We show by confocal microscopy and biochemical assays that FCRLA is a soluble resident endoplasmic reticulum (ER) protein, but it does not possess the amino acid sequence KDEL as an ER retention motif in its C-terminus. Using a series of deletion mutants, we found that its ER retention is most likely mediated by the amino terminal partial Ig-like domain. We have identified ER-localized Ig as the FCRLA ligand. FCRLA is unique among the large family of Fc receptors, in that it is capable of associating with multiple Ig isotypes, IgM, IgG and IgA. Among hemopoietic cells, FCRLA expression is restricted to the B lineage and is most abundant in germinal center B lymphocytes. The studies reported here demonstrate that FCRLA is more broadly expressed among human B lineage cells than originally reported; it is found at significant levels in resting blood B cells and at varying levels in all B-cell subsets in tonsil.

show abstract

Section: Fcrla Associates With Intracellular Igsupporting

confidence: 91%

FCRLA is a resident endoplasmic reticulum protein that associates with intracellular Igs, IgM, IgG and IgA

Santiago

Kulemzin

Reshetnikova

et al. 2010

International Immunology

View full text Add to dashboard Cite

show abstract

“…Surface expression of HLA-A, -B, and -C antigens is deficient in the Daudi cell line because of a deficiency of 832-microglobulin (36). That Daudi cells have membrane IgM but do not secrete it (37) suggests that Daudi may export A heavy chains by a class I-independent process or that the molecular defects in Daudi ((32 microglobulin deficiency) and in .221 (class I a-chain deficiency) may have different indirect effects on heavy-chain export.…”

mentioning

confidence: 99%

RETRACTED: Secretion and cell surface expression of IgG1 are impaired in human B lymphoblasts that lack HLA-A, -B, and -C antigens.

Burlingham

Ceman

DeMars

1989

Proc. Natl. Acad. Sci. U.S.A.

View full text Add to dashboard Cite

B-lymphoblastoid cell line (LCL) 721.221lacks HLA-A, -B, and -C class I antigens and transcripts as a result of -ray-induced mutations. LCL 721, from which mutant .221 was derived, produces membrane and secreted forms of IgGl(K). In contrast, IgG expression in .221 had these characteristics: (i) yl heavy chains were diminished by 98% but were detectable with chain-specific antibodies in cell lysates; (ii) K light chains were present at normal levels in cell lysates and free K chains were secreted; (iii) cell-surfaceassociated IgG and secreted IgG were absent. Mutants that had partially reduced amounts of class I antigens continued to secrete IgG; however, both the absolute amount ofIgG secreted and the relative amount of K vs. intact IgG secreted were abnormal in such partially class I-deficient cells. The failure to export IgG and the deficiency of HLA-A, -B, and -C were not merely coincidental in mutant .221, since production of IgG was restored by transferring a functional HLA-A, -B, or -C gene into .221. Cell surface antigen expression of cloned HLA-A, -B, and -C transgenes introduced into .221 was comparable to that of the same genes in their normal chromosomal locations. These observations reveal a relation between production of HLA class I gene products and production of IgG.Human class I histocompatibility (HLA) antigens are formed by noncovalent association between a polymorphic 44-kDa a-chain and nonpolymorphic 12-kDa P2-microglobulin. Class

show abstract

“…The round B-cell lines used in this study have been stably maintained as clonal populations for at least 12 years. LBW2 and LBW14 were derived by culturing PBLs from separate individuals with combined variable immunodeficiency in the presence of an unspecified strain of EBV (12,13). DB was generated under identical conditions with PBLs from a healthy individual (13).…”

Section: Materlals and Methodsmentioning

confidence: 99%

“…While the round B-cell lines were known to be EBNA positive by immunofluorescent staining (8,12), the nature of the infecting virus was ill defined, especially in the case of Josh 7 in which exogenous virus was not used in its generation. TIwo basic strains of EBV, types 1 and 2, exist worldwide.…”

Section: Materlals and Methodsmentioning

confidence: 99%

“…The LCLs used as controls in this work are typical latently infected LCLs and express EBV and cellular gene products in a manner consistent with published observations. LBW4, LBW25, and LBW26 were derived by EBV infection of juvenile bone marrow lymphocytes (LBW4) (17) or healthy adult PBLs (LBW25 and LBW26) (12). The LCL GM02292 was obtained from the NIGMS Human Genetic Mutant Cell Repository and carries an HGPRT mutation.…”

Section: Materlals and Methodsmentioning

confidence: 99%

See 1 more Smart Citation

Dual EBNA1 promoter usage by Epstein-Barr virus in human B-cell lines expressing unique intermediate cellular phenotypes

Taylor

Wetzel

Lyles

et al. 1994

J Virol

View full text Add to dashboard Cite

The use of different viral promoters for the expression of the EBNA1 gene product appears to be a critical step in the regulation of Epstein-Barr virus latent gene expression and may reflect the extent of differentiation of B-cell hosts. Low-passage Burkitt lymphoma cell lines resemble immature B cells in that they express CD10 (CALLA) and do not express B-cell activation antigens. In these cells, transcription from a promoter located in the BamHI F fragment of the viral genome results in the exclusive expression of EBNA1, referred to as the latency I pattern of viral gene expression. In contrast, high-passage Burkitt lymphoma cells and lymphoblastoid cell lines resemble activated B cells in that they do not express CD10 but do express activation antigens such as CD23. In these cells, the use of two promoters located in the BamHI W and C fragments of the viral genome leads to the expression of all six EBNA gene products (latency III). We have found that four human B-cell lines, DB, .LBW2, LBW14, and Josh 7, stably express a pattern of B-cell differentiation antigens intermediate between those found in latency I and latency Ill cell lines and characterized by the coexpression of CD10 and CD23. The pattern of EBNA1 promoter usage in these cell lines was examined to determine whether their intermediate cellular phenotype was reflected in their patterns of viral gene expression. DB, LBW2, and LBW14 utilize both the BamHI F promoter region and BamHI W promoter region to transcribe the EBNA1 gene..This stable pattern of mixed promoter usage for the expression of the EBNA gene products in B cells has not previously been described. In addition, these three B-cell lines expressed lower levels of the viral latent gene product EBNA2 than those typically observed in latency III cells. The lower levels of activation of viral and cellular promoters known to be regulated by EBNA2 also correlated with the reduced levels of EBNA2 expression in these cells. These included the viral LMP1 and LMP2A promoters and the cellular CD23B promoter. Thefourth B-cell line, Josh 7, expressed EBNA1 mRNAs derived from both the BamHI W promoter and BamHI C promoter, similar to latency III cells. The intermediate cellular phenotype in Josh 7 cells appeared to be due, in part, to a deficiency in the expression of viral LMP1. These results show that the B-cell lines express unique intermediate patterns of expression of viral and cellular gene products and suggest that a continuum of latency states may exist for Epstein-Barr virus-infected B lymphocytes.

show abstract

Differential regulation of membrane and secretory mu chain synthesis in human beta cell lines. Regulation of membrane mu or secreted mu.

Cited by 15 publications

References 42 publications

FCRLA is a resident endoplasmic reticulum protein that associates with intracellular Igs, IgM, IgG and IgA

FCRLA is a resident endoplasmic reticulum protein that associates with intracellular Igs, IgM, IgG and IgA

RETRACTED: Secretion and cell surface expression of IgG1 are impaired in human B lymphoblasts that lack HLA-A, -B, and -C antigens.

Dual EBNA1 promoter usage by Epstein-Barr virus in human B-cell lines expressing unique intermediate cellular phenotypes

Contact Info

Product

Resources

About