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Last update 08 May 2025

ATP11B

Last update 08 May 2025

Basic Info

Synonyms

ATP11B, ATPase class VI type 11B, ATPase IR

+ [7]

Introduction

Catalytic component of a P4-ATPase flippase complex which catalyzes the hydrolysis of ATP coupled to the transport of aminophospholipids, phosphatidylserines (PS) and phosphatidylethanolamines (PE), from the outer to the inner leaflet of intracellular membranes (PubMed:30018401). May contribute to the maintenance of membrane lipid asymmetry in endosome compartment (PubMed:30018401).

Drugs associated with ATP11B

CN118217404

Patent Mining

Target

ATP11B

Mechanism-

Active Org.

Shang Hai Sheng Yuan Hua An Sheng Wu Ke Ji You Xian Gong Si [+1]

Originator Org.

Shang Hai Sheng Yuan Hua An Sheng Wu Ke Ji You Xian Gong Si [+1]

Active Indication

disorder of aging [+1]

Inactive Indication-

Drug Highest PhaseDiscovery

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with ATP11B

100 Translational Medicine associated with ATP11B

0 Patents (Medical) associated with ATP11B

Literatures (Medical) associated with ATP11B

01 Apr 2025·MedComm

ATP11B Modulates Microglial Lipid Metabolism and Alleviates Alzheimer's Disease Pathology

Article

Author: Wu, Peiru ; Zhang, Yuchen ; Dong, Xin ; Zhao, Robert Chunhua ; Zhao, Xuyu ; Wang, Jiao ; Zhuang, Junyi ; Chao, Yufan ; Chen, Zixin ; Zhang, Shibo ; Ying, Yiwei ; Wu, Lingling

ABSTRACTAbnormal lipid metabolism in microglia leads to the formation of pathological lipid droplets (LDs), a phenomenon also observed in neurodegenerative diseases such as Alzheimer's disease (AD). The abnormal accumulation of LDs disrupts normal cellular function and exacerbates the pathological process of AD. ATP11B is a P4‐ATPase and the expression of Atp11b changes in the brain of patients with AD and diseases of lipid metabolism. The present study aimed to explore the regulatory role of ATP11B in microglial lipid metabolism and assess the potential of ATP11B as a therapeutic target for AD. Atp11b deficiency caused excessive fatty acid uptake and activated the PPAR signaling pathway, resulting in abnormal synthesis of neutral lipids and mitochondrial energy metabolism in microglia. Further results showed that Atp11b deficiency led to the accumulation of pathological LDs in microglia and AD mice. Conversely, overexpression of Atp11b alleviated exploratory behavior impairment, learning and memory impairment, LD accumulation, beta‐amyloid (Aβ) deposition, and inflammatory response in the brain of AD mice. These findings provide important clues for a better understanding of the pathogenesis of AD and for developing novel therapeutic strategies.

01 Dec 2024·Applied Microbiology and Biotechnology

CHO cell engineering via targeted integration of circular miR-21 decoy using CRISPR/RMCE hybrid system

Article

Author: Bayat, Hadi ; Ghanbari, Samaneh ; Mowla, Seyed Javad ; Davami, Fatemeh ; Adibzadeh, Setare ; Barkhordari, Farzaneh ; Amiri, Shahin ; Faghihi, Faezeh

AbstractChinese hamster ovary (CHO) cells, widely acknowledged as the preferred host system for industrial recombinant protein manufacturing, play a crucial role in developing pharmaceuticals, including anticancer therapeutics. Nevertheless, mammalian cell-based biopharmaceutical production methods are still beset by cellular constraints such as limited growth and poor productivity. MicroRNA-21 (miR-21) has a major impact on a variety of malignancies, including glioblastoma multiforme (GBM). However, reduced productivity and growth rate have been linked to miR-21 overexpression in CHO cells. The current study aimed to engineer a recombinant CHO (rCHO) cell using the CRISPR-mediated precise integration into target chromosome (CRIS-PITCh) system coupled with the Bxb1 recombinase-mediated cassette exchange (RMCE) to express a circular miR-21 decoy (CM21D) with five bulged binding sites for miR-21 sponging. Implementing the ribonucleoprotein (RNP) delivery method, a landing pad was inserted into the genome utilizing the CRIS-PITCh technique. Subsequently, the CM21D cassette flanked by Bxb1 attB was then retargeted into the integrated landing pad using the RMCE/Bxb1 system. This strategy raised the targeting efficiency by 1.7-fold, and off-target effects were decreased. The miR-21 target genes (Pdcd4 and Atp11b) noticed a significant increase in expression upon the miR-21 sponging through CM21D. Following the expression of CM21D, rCHO cells showed a substantial decrease in doubling time and a 1.3-fold increase in growth rate. Further analysis showed an increased yield of hrsACE2, a secretory recombinant protein, by 2.06-fold. Hence, we can conclude that sponging-induced inhibition of miR-21 may lead to a growth rate increase that could be linked to increased CHO cell productivity. For industrial cell lines, including CHO cells, an increase in productivity is crucial. The results of our research indicate that CM21D is an auspicious CHO engineering approach.Key points• CHO is an ideal host cell line for producing industrial therapeutics manufacturing, and miR-21 is downregulated in CHO cells, which produce recombinant proteins.• The miR-21 target genes noticed a significant increase in expression upon the miR-21 sponging through CM21D. Additionally, sponging of miR-21 by CM21D enhanced the growth rate of CHO cells.• Productivity and growth rate were increased in CHO cells expressing recombinant hrs-ACE2 protein after CM21D knocking in.Graphical abstract

15 Dec 2022·Biology Open

A genome-wide CRISPR screen implicates plasma membrane asymmetry in exogenous C6-ceramide toxicity

Article

Author: Lange, Mike ; Olzmann, James A. ; Deol, Kirandeep K. ; Morris, Siti Nur Sarah

ABSTRACTThe bioactive sphingolipid ceramide impacts diverse cellular processes (e.g. apoptosis and cell proliferation) through its effects on membrane dynamics and intracellular signaling pathways. The dysregulation of ceramide metabolism has been implicated in cancer evasion of apoptosis and targeting ceramide metabolism has potential therapeutic benefits as a strategy to kill cancer cells and slow tumor growth. However, the mechanisms of cancer cell resistance to ceramide-mediated cell death are vastly intertwined and incompletely understood. To shed light on this mystery, we performed a genome-wide CRISPR-Cas9 screen to systematically identify regulators of cancer resistance to the soluble short chain ceramide, C6 ceramide (C6-Cer). Our results reveal a complex landscape of genetic modifiers of C6-Cer toxicity, including genes associated with ceramide and sphingolipid metabolism, vesicular trafficking, and membrane biology. Furthermore, we find that loss of the phospholipid flippase subunit TMEM30A impairs the plasma membrane trafficking of its binding partner, the P4-type ATPase ATP11B, and depletion of TMEM30A or ATP11B disrupts plasma membrane asymmetry and promotes resistance to C6-Cer toxicity. Together, our findings provide a resource of genetic modifiers of C6-Cer toxicity and reveal an unexpected role of plasma membrane asymmetry in C6-Cer induced cell death.

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ATP11B

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