Last update 01 Nov 2024

ITM2B

Last update 01 Nov 2024

Basic Info

Synonyms

ABri23, BRI, BRI2

+ [19]

Introduction

Plays a regulatory role in the processing of the amyloid-beta A4 precursor protein (APP) and acts as an inhibitor of the amyloid-beta peptide aggregation and fibrils deposition. Plays a role in the induction of neurite outgrowth. Functions as a protease inhibitor by blocking access of secretases to APP cleavage sites. Mature BRI2 (mBRI2) functions as a modulator of the amyloid-beta A4 precursor protein (APP) processing leading to a strong reduction in the secretion of secretase-processed amyloid-beta protein 40 and amyloid-beta protein 42. Bri23 peptide prevents aggregation of APP amyloid-beta protein 42 into toxic oligomers.

Drugs associated with ITM2B

WO2022218499

Patent Mining

Target

ITM2B

Mechanism-

Active Org.

Alpha Beta Ltd.

Originator Org.

Alpha Beta Ltd.

Active Indication

Dementia

Inactive Indication-

Drug Highest PhaseDiscovery

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with ITM2B

100 Translational Medicine associated with ITM2B

0 Patents (Medical) associated with ITM2B

385

Literatures (Medical) associated with ITM2B

28 Oct 2024·Journal of Chemical Information and Modeling

Deciphering the Morphological Difference of Amyloid-β Fibrils in Familial and Sporadic Alzheimer’s Diseases

Article

Author: Ding, Feng ; Song, Zhiyuan ; Huang, Gangtong ; Xu, Yun ; Sun, Yunxiang

The aggregation of amyloid-β (Aβ) into amyloid fibrils is the major pathological hallmark of Alzheimer's disease (AD). Aβ fibrils can adopt a variety of morphologies, the relative populations of which are recently found to be associated with different AD subtypes such as familial and sporadic AD (fAD and sAD, respectively). The two AD subtypes differ in their ages of onset, AD-related genetic predispositions, and dominant Aβ fibril morphologies. We postulate that these disease subtype-dependent fibril morphology differences can be attributed to the intrinsic fibril properties and interacting molecules in the environment. Using atomistic discrete molecular dynamics simulations, we demonstrated that the fAD-dominant morphology exhibited a lower free-energy barrier for fibril growth but also a lower stability compared with the sAD-dominant fibril morphology, resulting in the time-dependent population change consistent with experimental observations. Additionally, we studied the effect of the Bri2 BRICHOS domain, an endogenous protein that has been reported to inhibit Aβ aggregation by preferential binding to fibrils, as one of the possible environmental factors. The Bri2 BRICHOS domain showed stronger binding to the fAD-dominant fibril than the sAD-dominant fibril in silico, suggesting a more effective suppression of fAD-dominant fibril formation. This result explains the high population of the sAD-dominant fibril morphology in sporadic cases with normal Bri2 functions. Genetic predisposition in fAD, on the other hand, might impair or overwhelm Bri2 functions, leading to a high population of fAD-associated fibril morphology. Together, our computational findings provide a theoretical framework for elucidating the AD subtypes entailed by distinct dominant amyloid fibril morphologies.

01 Aug 2024·Ecology and Evolution

A comparison of the large‐scale gene expression patterns in summer and fall migratory Pantala flavescens (Fabricius) in northern China

Article

Author: Wang, Na ; Cao, Lingzhen

AbstractPantala flavescens (Fabricius) is the most well‐known seasonal migratory insect. This research focused on the molecular response of P. flavescens migration in summer and fall. A total of 17,810 assembled unigenes were obtained and 624 differentially expressed genes (DEGs) were identified in summer migration compared to fall migration. A number of DEGs, including cpr49Ae, itm2b, chitinase, cpr11B, laccase2, nd5, vtg2 and so on, had previously been reported to be involved in cold‐ and high‐temperature resistance. Functional enrichment analysis showed three pathways ‘that antibacterial humoral response, response to bacterial, and lipid transporter activity’ were significantly enriched in summer migration while that six pathways ‘structural constituent of cuticle, chitin binding, mitochondrion, propanoate metabolism, citrate cycle, hypertrophic cardiomyopathy’ were significantly enriched in fall migration. These results will provide a valuable baseline for further understanding of the molecular mechanisms of insect adaptation to different climate migrations.

01 Aug 2024·Pathology International

Exosomal miR‐196a‐5p contributes to esophageal squamous cell carcinoma malignant progression by inhibiting ITM2B

Article

Author: Zhang, Fan ; Cai, Jun ; Zhu, Yan ; Li, Shuang ; Zeng, Hai ; Huang, Min

AbstractExosomes from cancer cells function as carriers to spread or transport specific microRNAs (miRNAs) to distant sites to exert their effects, but the mechanism of exosomal miRNA action in esophageal squamous cell carcinoma (ESCC) has not been fully explained. Therefore, in this study, we were interested in the impact of exosomal miR‐196a‐5p in ESCC progression. We found that miR‐196a‐5p was expressed enriched in clinical tissues, ESCC cells, and exosomes. Functionally, depletion of miR‐196a‐5p impeded ESCC cell growth, migration, and invasion, whereas overexpression of miR‐196a‐5p produced the opposite results. Moreover, enhancement of exosomal miR‐196a‐5p in recipient ESCC cells triggered more intense proliferation and migration. Mechanistically, we identified integral membrane protein 2B (ITM2B) as a direct target of miR‐196a‐5p. Silencing of ITM2B partially counteracted the inhibitory effect of miR‐196a‐5p inhibitors on the malignant phenotype of ESCC. Furthermore, in vivo, lower miR‐196a‐5p levels triggered by the introduction of antagomiR‐196a‐5p resulted in the generation of smaller volume and weight xenograft tumors. Thus, our results demonstrated novel mechanisms of exosomal and intracellular miR‐196a‐5p‐mediated ESCC growth and migration and identify the interaction of miR‐196a‐5p with ITM2B. These works might provide new targets and basis for the development of clinical treatment options for ESCC.

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ITM2B

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