EHBP1L1

Last update 08 May 2025

Basic Info

Synonyms

DKFZp762C186, EH domain binding protein 1 like 1, EH domain-binding protein 1-like protein 1

+ [2]

Introduction

May act as Rab effector protein and play a role in vesicle trafficking.

100 Clinical Results associated with EHBP1L1

100 Translational Medicine associated with EHBP1L1

0 Patents (Medical) associated with EHBP1L1

Literatures (Medical) associated with EHBP1L1

12 Mar 2024·Blood Advances

Wu J, Moriwaki K, Asuka T, et al. EHBP1L1, an apicobasal polarity regulator, is critical for nuclear polarization during enucleation of erythroblasts. Blood Adv. 2023;7(14):3382–3394.

Article

25 Jul 2023·Blood Advances

EHBP1L1, an apicobasal polarity regulator, is critical for nuclear polarization during enucleation of erythroblasts

Article

Author: Taniguchi, Manabu ; Kunii, Masataka ; Moriwaki, Kenta ; Wu, Ji ; Nagasawa, Takashi ; Miyoshi, Eiji ; Sugiyama, Tatsuki ; Kanda, Satoshi ; Yoshimura, Shin-ichiro ; Asuka, Tatsuya ; Hosen, Naoki ; Harada, Akihiro ; Nakai, Ritsuko

AbstractCell polarity, the asymmetric distribution of proteins and organelles, is permanently or transiently established in various cell types and plays an important role in many physiological events. epidermal growth factor receptor substrate 15 homology domain-binding protein 1–like 1 (EHBP1L1) is an adapter protein that is localized on recycling endosomes and regulates apical-directed transport in polarized epithelial cells. However, the role of EHBP1L1 in nonepithelial cells, remains unknown. Here, Ehbp1l1−/− mice showed impaired erythroblast enucleation. Further analyses showed that nuclear polarization before enucleation was impaired in Ehbp1l1−/− erythroblasts. It was also revealed that EHBP1L1 interactors Rab10, Bin1, and dynamin were involved in erythroblast enucleation. In addition, Ehbp1l1−/− erythrocytes exhibited stomatocytic morphology and dehydration. These defects in erythroid cells culminated in early postnatal anemic lethality in Ehbp1l1−/− mice. Moreover, we found the mislocalization of nuclei and mitochondria in the skeletal muscle cells of Ehbp1l1−/− mice, as observed in patients with centronuclear myopathy with genetic mutations in Bin1 or dynamin 2. Taken together, our findings indicate that the Rab8/10-EHBP1L1-Bin1-dynamin axis plays an important role in multiple cell polarity systems in epithelial and nonepithelial cells.

01 Apr 2023·Advanced Science

EHBP1L1 Drives Immune Evasion in Renal Cell Carcinoma through Binding and Stabilizing JAK1

Article

Author: Liu, Huashan ; Chen, Minyu ; Huang, Kangbo ; Wang, Yinghan ; Feng, Zihao ; Deng, Qiong ; Gui, Chengpeng ; Yang, Jiefeng ; Jin, Xiaohan ; Shu, Guannan ; Wang, Zhu ; Luo, Junhang ; Fu, Liangmin ; Zhou, Xinwei ; Lu, Jun ; Li, Jiaying ; Chen, Zhenhua ; Wei, Jinhuan ; Pan, Yihui ; Li, Pengju ; Zhang, Jiaxing ; Cen, Junjie ; Xu, Quanhui ; Chen, Wei ; Liang, Hui

AbstractHigh lymphocyte infiltration and immunosuppression characterize the tumor microenvironment (TME) in renal cell carcinoma (RCC). There is an urgent need to elucidate how tumor cells escape the immune attack and to develop novel therapeutic targets to enhance the efficacy of immune checkpoint blockade (ICB) in RCC. Overactivated IFN‐γ‐induced JAK/STAT signaling involves in such TME, but the underlying mechanisms remain elusive. Here, EH domain‐binding protein 1‐like protein 1 (EHBP1L1) is identified as a crucial mediator of IFN‐γ/JAK1/STAT1/PD‐L1 signaling in RCC. EHBP1L1 is highly expressed in RCC, and high EHBP1L1 expression levels are correlated with poor prognosis and resistance to ICB. EHBP1L1 depletion significantly inhibits tumor growth, which is attributed to enhanced CD8+ T cell‐mediated antitumor immunity. Mechanistically, EHBP1L1 interacts with and stabilizes JAK1. By competing with SOCS1, EHBP1L1 protects JAK1 from proteasomal degradation, which leads to elevated JAK1 protein levels and JAK1/STAT1/PD‐L1 signaling activity, thereby forming an immunosuppressive TME. Furthermore, the combination of EHBP1L1 inhibition and ICB reprograms the immunosuppressive TME and prevents tumor immune evasion, thus significantly reinforcing the therapeutic efficacy of ICB in RCC patient‐derived xenograft (PDX) models. These findings reveal the vital role of EHBP1L1 in immune evasion in RCC, which may be a potential complement for ICB therapy.

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EHBP1L1

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