2023年2月13日 · Here, we report cryo-EM structures of the EGF- and epiregulin-bound EGFR/HER2 ectodomain complexes at resolutions of 3.3 Å and 4.5 Å, respectively. Together with the functional analyses, we...

EGFR（英语：epidermal growth factor receptor，简称为EGFR、ErbB-1或HER1）是表皮生长因子受体（HER）家族成员之一。该家族包括HER1（erbB1，EGFR）、HER2（erbB2，NEU）、HER3（erbB3）及HER4（erbB4）。HER家族在细胞生理过程中发挥重要的调节作用。

2024年12月16日 · 它们和EGFR同家族，但功能却并不相同： HER2无胞外配体； HER3无胞内激酶活性； HER4功能复杂，既促进癌症发生，也诱导癌细胞凋亡。 ERBB 是一类原癌基因家族，全称为 “v-erb-b erythroblastic leukemia viral oncogene homolog”（禽类成红细胞白血病病毒 v-erb-B 癌基因同源物）人表皮生长因子受体家族（ErbB receptor family），命名来源于对禽类红细胞白血病病毒的研究。 在哺乳动物细胞中存在与之同源的基因，即 ERBB 基因家族，包括ErbB-1（ …

2023年2月25日 · EGFR与HER2相互作用弱是影响复合物稳定性和结构解析的关键因素。作者巧妙地在EGFR和HER2蛋白的胞内区域添加了两段电性相反的coiled-coil肽段，利用二者的静电相互作用稳定了EGFR/HER2复合物。

2021年11月14日 · her蛋白是一个受体酪氨酸激酶家族，在正常和肿瘤细胞生物学中都发挥着作用。该家族包括四个高度同源的成员：egfr（erbb1/her1）、her2(erbb2)、her3(erbb3)和her4(erbb4)，它们都由四部分组成：配体结合的细胞外结…

2024年11月19日 · We hypothesize that epidermal growth factor receptor (EGFR), a dimerization partner of HER2, can modulate HER2 trafficking through endocytic pathways and affect T-DXd uptake. We demonstrate that elevated EGFR expression levels can promote EGFR/HER2 heterodimer formation and suppress T-DXd internalization and efficacy.

In contrast to other active receptors, HER3 becomes a powerful signaling agent when paired with receptors like HER2, EGFR, and MET, leading to resilient growth signals that resist targeted therapies. A study on ALK inhibitors in ALK+ NSCLC unveiled HER3’s involvement in resistance.

Here, we report cryo-EM structures of the EGF- and epiregulin-bound EGFR/HER2 ectodomain complexes at resolutions of 3.3 Å and 4.5 Å, respectively. Together with the functional analyses, we demonstrate that only the dimerization arm of HER2, but not that of EGFR, is essential for their heterodimer formation and signal transduction.

2024年11月15日 · Through dimerization with non-EGFR receptors (HER2 and MET receptor, for example), HER3 can produce resistance to EGFR targeted therapy [51]. For instance, in head and neck and BCs, resistance to EGFR tyrosine kinase inhibitors (TKI) is associated with HER2-HER3 mediated signaling [ 52 ].

Although HER3 does not cause tumorigenesis on its own, HER2:HER3 heterodimers possess the highest transforming capability among all the possible EGFR family dimers (30,31). The superior oncogenic capability of the dimer pair makes HER3 critical for HER2-mediated tumorigenesis in multiple tumor types.