CD antigens 1993

Division of Tumor Immunology, Dana-Farber Cancer Institute, Boston, MA 02115.
Blood (Impact Factor: 10.45). 03/1994; 83(4):879-80. DOI: 10.3109/10428199409052676
Source: PubMed
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    • "The mAbs used in this study were human integrin α3 mAb X8 [44], human integrin α5 mAb PUJ-2 [45], human integrin β1 mAb A1A5 and TS2/16 [46], human CD81 mAb M38 [47], human KAI1/CD82 mAbs M104 [47], 4F9 [14], [48], and TS82b (Tepnel, Stamford, CT), phosphotidylinositol 4, 5-biphosphate (PIP2) mAb (Assay Designs Inc., Ann Arbor, MI), and β-tubulin mAb (Sigma, St. Louis, MO). A mouse monoclonal IgG2 was used as a negative control antibody (Sigma). "
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    ABSTRACT: To determine how tetraspanin KAI1/CD82, a tumor metastasis suppressor, inhibits cell migration, we assessed which cellular events critical for motility are altered by KAI1/CD82 and how KAI1/CD82 regulates these events. We found that KAI1/CD82-expressing cells typically exhibited elongated cellular tails and diminished lamellipodia. Live imaging demonstrated that the polarized protrusion and retraction of the plasma membrane became deficient upon KAI1/CD82 expression. The deficiency in developing these motility-related cellular events was caused by poor formations of actin cortical network and stress fiber and by aberrant dynamics in actin organization. Rac1 activity was reduced by KAI1/CD82, consistent with the diminution of lamellipodia and actin cortical network; while the growth factor-stimulated RhoA activity was blocked by KAI1/CD82, consistent with the loss of stress fiber and attenuation in cellular retraction. Upon KAI1/CD82 expression, Rac effector cofilin was not enriched at the cell periphery to facilitate lamellipodia formation while Rho kinase exhibited a significantly lower activity leading to less retraction. Phosphatidylinositol 4, 5-biphosphate, which initiates actin polymerization from the plasma membrane, became less detectable at the cell periphery in KAI1/CD82-expressing cells. Moreover, KAI1/CD82-induced phenotypes likely resulted from the suppression of multiple signaling pathways such as integrin and growth factor signaling. In summary, at the cellular level KAI1/CD82 inhibited polarized protrusion and retraction events by disrupting actin reorganization; at the molecular level, KAI1/CD82 deregulated Rac1, RhoA, and their effectors cofilin and Rho kinase by perturbing the plasma membrane lipids.
    PLoS ONE 12/2012; 7(12):e51797. DOI:10.1371/journal.pone.0051797 · 3.23 Impact Factor
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    04/2001; 17(1).
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    ABSTRACT: We determined the complete genomic sequence of the human CD79b (Ig beta/B29) gene. The CD79b gene product is associated with the membrane immunoglobulin signaling complex which is composed of immunoglobulin (Ig) itself, associated in a noncovalent fashion with CD79b and a second polypeptide chain, CD79a (Ig alpha/mb1). The sequence and exon/intron organization of the human and mouse CD79b genes are highly similar. The gene organization suggests that some variant forms of CD79b may arise by virtue of alternative splicing of mRNA. In addition, a number of conserved regulatory sequences commonly found in Ig genes are present in sequences which flank the human CD79b gene. Some of these sequences are distinct from those found in the CD79a promoter. These differences may explain why transcription of CD79b, but not CD79a, is observed in plasma cells. A new Taq 1 restriction fragment length polymorphism is described that is not associated with any structural polymorphisms of the expressed CD79b polypeptide.
    Immunogenetics 02/1994; 40(2):145-9. DOI:10.1007/BF00188178 · 2.23 Impact Factor
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