CD79B
小结
CD79B是致癌基因，CD79B编码蛋白为一种表面免疫球蛋白，与CD79A形成复合物，并构成B细胞受体（BCR）的一部分。CD79(Iga/Igb)复合物对于BCR信号通路很重要，在B细胞整个发育过程中为其成熟和存活作支撑。CD79B的细胞质部分含有由Src原癌基因家族蛋白激酶磷酸化的免疫受体酪氨酸基激活基序（ITAM）。这些区域用作信号转导复合物与激酶（SYK）以及信号调节的对接位点。在弥漫性大B细胞淋巴瘤中，特别是激活的B细胞样亚型中检测到CD79B的激活突变。CD79B突变导致表面BCR表达增加，降低BCR内化和抑制Lyn（Lyn原癌基因）激酶反馈抑制，从而导致BCR信号传导增加。CD79B的胚系突变导致丙种球蛋白血症，是一种严重的B细胞功能障碍的免疫缺陷综合征。CD79B在弥漫性大B细胞淋巴瘤中反复发生改变。
CD79B is a surface immunoglobulin that forms a complex with CD79A to form a component of the B-cell receptor (BCR). The CD79 (Iga/Igb) complex is important for signaling from the BCR to support maturation and survival of B-cells throughout development . The cytoplasmic portion of CD79B contains immunoreceptor tyrosine-based activation motif (ITAM) domains that become phosphorylated by SRC proto-oncogene family protein kinases. These regions serve as docking sites for signaling complex formation with kinases such as SYK (spleen tyrosine kinase) and for signal regulation. Activating mutations of CD79B have been identified in diffuse large B-cell lymphoma, particularly the activated B-cell-like subtype suggesting that CD79B acts as an oncogene. CD79B mutations result in increased surface BCR expression, reduced BCR internalization and dampening of LYN (Lyn proto-oncogene) kinase feedback inhibition, thus resulting in increased BCR signaling. Somatic mutation in the protein's ITAM domain have also been identified and shown to affect signaling. Germline CD79B mutation leads to agammaglobulinemia, a severe immunodeficiency syndrome with B-cell dysfunction. Antibody-drug conjugates targeting CD79B and inhibitors targeting SRC activity, such as dasatinib, can reduce BCR signaling.