Search PubMed⌕ Search

PubMed · 7561359

[Immunoglobulin abnormalities].

Abstract

The source did not provide an abstract. Follow the original record for more information.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

M Kosaka, M Takishita. 1995-07-10. [Immunoglobulin abnormalities].. https://pubmed.ncbi.nlm.nih.gov/7561359/

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

Shift of immunoglobulin phenotypes in B-cell precursor cell lines.

Rearrangement of immunoglobulin chain genes is a hallmark of mammalian B cell development and differential expression of immunoglobulin chains has aided in the diagnosis and prognostication of patients with ALL. Matsu et al. describe two novel precursor B-cell lines with shift of expression of immunoglobulin phenotypes at diagnosis and relapse. The impact of this observation on diagnosis and the elucidation of the biology of the neoplastic cells will be discussed.

B-Lymphocytes↗

The Epstein-Barr virus latent membrane protein 1 putative Janus kinase 3 (JAK3) binding domain does not mediate JAK3 association or activation in B-lymphoma or lymphoblastoid cell lines.

Epstein-Barr virus (EBV) latent infection membrane protein 1 (LMP1) has an intermediate domain between the two cytoplasmic carboxyl-terminal domains that are critical for transforming B-lymphocytes into lymphoblastoid cell lines (LCLs). The intermediate domain has been implicated in Janus kinase 3 (JAK3) association and activation. We now find that LCLs transformed by EBV recombinants that express Flag-LMP1 with the putative JAK3 binding and activating intermediate domain deleted and LCLs transformed by Flag-LMP1 EBV recombinants have similar levels of phosphotyrosine-activated JAK3, signal transducer and activator of transcription 3 (STAT3), or STAT5 and similar very low levels of JAK3 associated with LMP1. Further, transient Flag-LMP1 expression in a B-lymphoma cell line transduces signals that upregulate TRAF1 levels but does not alter JAK3 levels or activation state. Although these data indicate that the LMP1 putative JAK3 binding and activating intermediate domain does not mediate JAK3 association or activation in B-lymphocytes, JAK3 association with LMP1 could be significant, particularly in cells in which LMP1, JAK3, or a JAK3-associated protein is expressed at high levels.

B-Lymphocytes↗

CR2/CD21 proximal promoter activity is critically dependent on a cell type-specific repressor.

Transcription of the human complement receptor type 2 (CR2/CD21) gene is controlled by both proximal promoter and intronic elements. CR2 is primarily expressed on B cells from the immature through mature cell stages. We have previously described the presence of an intronic element that is required for both cell- and stage-specific expression of CR2. In this study, we report the identification of a cell type-specific repressor element within the proximal promoter. This repressor sequence is shown by linker scanning mutagenesis to comprise an E box motif. By supershift analysis this element binds members of the basic helix-loop-helix family of proteins, in particular E2A gene products. Mutational analysis demonstrates that binding of E2A proteins is critical for functioning of this repressor. Thus, E2A activity is key not only for early B cell development, but also for controlling CR2 expression, a gene expressed only during later stages of ontogeny.

B-Lymphocytes↗