MAL

Last update 08 May 2025

Basic Info

Synonyms

MAL, mal, T cell differentiation protein, MVP17

+ [3]

Introduction

Could be an important component in vesicular trafficking cycling between the Golgi complex and the apical plasma membrane. Could be involved in myelin biogenesis and/or myelin function.

100 Clinical Results associated with MAL

100 Translational Medicine associated with MAL

0 Patents (Medical) associated with MAL

1,197

Literatures (Medical) associated with MAL

23 Apr 2025·ACS Applied Materials & Interfaces

Engineered NK Exosomes Captured Antigens In Situ for Enhanced Tumor Immunotherapy

Article

Author: Tang, Junjie ; Liu, Zhuoyin ; Cheng, Lili ; Xue, Yifan ; Peng, Dan ; Liu, Jie

Natural killer (NK) cells are widely involved in the field of tumor immunotherapy due to their unique killing ability. However, the durability and efficacy of NK-cell monotherapy are facing great challenges owing to the limitation of immunosuppressive tumor microenvironment (TME). NK cell-derived exosomes (Neo) not only play an innate immunomodulatory role similar to NK cells but also emerge as promising antitumor nanocarriers. In this study, an engineered Neo (R@Neo-MN) was designed that encapsulates the multifunctional antitumor drug (Raddeanin a, RA) and modified with maleimide (Mal, M) and mannose (Man, N). The obtained R@Neo-MN could not only exert NK cell-like antitumor function but also induce the immunogenic cell death of tumors to release tumor-associated antigens (TAAs). Furthermore, R@Neo-MN activated the cyclic guanosine monophosphate-adenosine monophosphate synthase/interferon gene stimulator (cGAS/STING) to release type I interferons (IFN). Then, R@Neo-MN could capture TAAs through Mal and specifically target dendritic cells (DCs) through Man, thereby promoting the maturation of DCs and enhancing tumor-specific cytotoxic T-cell (CTL)-mediated adaptive immunity. The released IFN further promoted the infiltration and activition of NK cells and CTLs at the tumor site. Our study suggested a novel strategy that harnesses both innate and adaptive immunity for enhanced tumor immunotherapy.

01 Feb 2025·Translational Stroke Research

Modulation of the Immunological Milieu in Acute Aneurysmal Subarachnoid Hemorrhage: The Potential Role of Monocytes Through CXCL10 Secretion

Article

Author: Sanchez, Sebastian ; Gudino, Andres ; Sagues, Elena ; Lu, Yongjun ; Samaniego, Edgar A ; Hasan, David ; Chimenti, Michael S ; Dier, Carlos

Emerging evidence indicates that aneurysmal subarachnoid hemorrhage (aSAH) elicits a response from both innate and adaptive immune systems. An upregulation of CD8 + CD161 + cells has been observed in the cerebrospinal fluid (CSF) after aSAH, yet the precise role of these cells in the context of aSAH is unkown. CSF samples from patients with aSAH and non-aneurysmal SAH (naSAH) were analyzed. Single-cell RNA sequencing (scRNAseq) was performed on CD8 + CD161 + sorted samples from aSAH patients. Cell populations were identified using "clustering." Gene expression levels of ten previously described genes involved in inflammation were quantified from aSAH and naSAH samples using RT-qPCR. The study focused on the following genes: CCL5, CCL7, APOE, SPP1, CXCL8, CXCL10, HMOX1, LTB, MAL, and HLA-DRB1. Gene clustering analysis revealed that monocytes, NK cells, and T cells expressed CD8 + CD161 + in the CSF of patients with aSAH. In comparison to naSAH samples, aSAH samples exhibited higher mRNA levels of CXCL10 (median, IQR = 90, 16-149 vs. 0.5, 0-6.75, p = 0.02). A trend towards higher HMOX1 levels was also observed in aSAH (median, IQR = 12.6, 9-17.6 vs. 2.55, 1.68-5.7, p = 0.076). Specifically, CXCL10 and HMOX1 were expressed by the monocyte subpopulation. Monocytes, NK cells, and T cells can potentially express CD8 + CD161 + in patients with aSAH. Notably, monocytes show high levels of CXCL10. The elevated expression of CXCL10 in aSAH compared to naSAH indicates its potential significance as a target for future studies.

14 Jan 2025·Proceedings of the National Academy of Sciences

Structural basis for TIR domain–mediated innate immune signaling by Toll-like receptor adaptors TRIF and TRAM

Article

Author: Kobe, Bostjan ; Manik, Mohammad K. ; Hedger, Andrew ; Kim, Hyoyoung ; Lee, Morris Y. L. ; Pan, Mengqi ; Nanson, Jeffrey D. ; Qian, Xiaoqi ; Wu, Hao ; Stacey, Katryn J. ; Vajjhala, Parimala R. ; Ve, Thomas ; Raunser, Stefan ; Xiao, Le ; Landsberg, Michael J. ; Pospich, Sabrina ; Gu, Weixi

Innate immunity relies on Toll-like receptors (TLRs) to detect pathogen-associated molecular patterns. The TIR (Toll/interleukin-1 receptor) domain-containing TLR adaptors TRIF (TIR domain–containing adaptor-inducing interferon-β) and TRAM (TRIF-related adaptor molecule) are essential for MyD88-independent TLR signaling. However, the structural basis of TRIF and TRAM TIR domain–based signaling remains unclear. Here, we present cryo-EM structures of filaments formed by TRIF and TRAM TIR domains at resolutions of 3.3 Å and 5.6 Å, respectively. Both structures reveal two-stranded parallel helical arrangements. Functional studies underscore the importance of intrastrand interactions, mediated by the BB-loop, and interstrand interactions in TLR4-mediated signaling. We also report the crystal structure of the monomeric TRAM TIR domain bearing the BB loop mutation C117H, which reveals conformational differences consistent with its inactivity. Our findings suggest a unified signaling mechanism by the TIR domains of the four signaling TLR adaptors MyD88, MAL, TRIF, and TRAM and reveal potential therapeutic targets for immunity-related disorders.

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MAL

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