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Last update 08 May 2025

PACC1

Last update 08 May 2025

Basic Info

Synonyms

Acid-sensitive outwardly-rectifying anion channel, ASOR, C1orf75

+ [11]

Introduction

Chloride channel gated by pH that facilitates the entry of chloride ions into cells upon exposure to extracellular acidic pH (PubMed:31023925, PubMed:31318332). Involved in acidosis-induced cell death by mediating chloride influx and subsequent cell swelling (PubMed:31023925, PubMed:31318332).

Drugs associated with PACC1

TXP1-ASO

Target

PACC1

Mechanism

PACC1 modulators

Active Org.

Ossianix, Inc.

Originator Org.

Ossianix, Inc.

Active Indication-

Inactive Indication-

Drug Highest PhaseDiscovery

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with PACC1

100 Translational Medicine associated with PACC1

0 Patents (Medical) associated with PACC1

1,477

Literatures (Medical) associated with PACC1

01 Aug 2025·Water Research

Binding interaction between chlorine and powder activated carbon driving nonradical oxidation toward diclofenac abatement: Surface-bound complexes generating on diverse sites performing diverse duties

Article

Author: Liu, Baicang ; Wang, Ying ; Liu, Wen ; Chen, Xin ; Yang, Chunyan ; Ma, Jun ; Cheng, Xin ; Chen, Liang ; Chen, Guijing ; Kalonji, Gretchen

Photolysis of chlorine by UV irradiation is commonly used as an advanced oxidation process for the abatement of micropollutants, but suffers from the energy-extensive consumption and potential risk, e.g., formation of disinfection byproduct and use of fragile mercury-containing lamps. This study demonstrates powder activated carbon (PAC) catalysis-mediated chlorine activation to significantly promote the degradation of diclofenac (DCF), a representative emerging contaminant, via nonradical oxidation pathways, thus reconsidering the interaction between PAC and chlorine in depth which are widely applied in actual water treatment. The chlorine/PAC process produces reactive metastable surface-bound complexes, i.e., PAC-HOCl*, via the cleavage of O-Cl bond in chlorine and formation of C-Cl by interfacial binding interaction, to regulate the charge distribution and electron density configuration. Carbonyl groups and structural defects of PAC are determined as the active sites via functional group derivatization and defect engineering for PAC modification, and performed diverse duties in the chlorine activation, producing PAC-C=O-HOCl* and PAC-D-HOCl*, responsible for the oxidation ability improvement and electron transfer acceleration, respectively. Of particular significance is that the chlorine/PAC process performs high efficiencies in the degradation of diverse micropollutants and is scarcely affected by water matrices, exhibiting a high potential of practical application for the decontamination of emerging micropollutants without the requirement of external energy input.

01 Jul 2025·Brain, Behavior, and Immunity

Astrocyte elevated gene-1 (AEG-1) in myeloid cells is a key driver for the development of chemotherapy-induced peripheral neuropathy

Article

Author: Sarkar, Devanand ; Bryan, Tayla ; Damaj, M Imad ; Herz, Sara M ; Mckiver, Bryan D ; Salem, Aliasger K ; Poklis, Justin L ; Bigbee, John W ; Windle, Jolene J ; Patel, Shivani ; Mann, Jared

Chemotherapy-induced peripheral neuropathy (CIPN) is a dose-limiting side effect of chemotherapy treatment, often resulting in the discontinuation of treatment. Paclitaxel activates peripheral macrophages, generating a neuroinflammatory response that contributes to CIPN development and maintenance. Astrocyte Elevated Gene-1 (AEG-1), also known as Metadherin or LYRIC, is a multifunctional protein that modulates macrophage activity and regulates inflammation through direct interaction with NF-κB, a transcriptional regulator of proinflammatory cytokine/chemokine (PIC) expression. We aimed to determine whether AEG-1 contributes to the development and maintenance of CIPN pathologies by using both global (AEG-1 KO) and myelocyte-specific knockout (AEG-1ΔMAC) transgenic mouse strains in an animal model of CIPN that replicates specific human clinical phenotypes. We hypothesized that inhibition of AEG1 expression in myeloid cells, such as monocytes and macrophages, would prevent the development and maintenance of CIPN. Our results showed that global AEG-1 deletion prevented the development of CIPN pathologies induced by PAC, as well as oxaliplatin (OHP). PAC treatment was found to increase AEG-1 and PIC expression in the DRGs of WT mice and in peritoneal macrophages isolated from C57BL/6J mice. However, in the absence of AEG-1 expression, PAC-induced neuroinflammation was completely halted in the DRGs of AEG-1 KO mice. This preventative phenotype and PIC expression profile was mirrored in AEG-1ΔMAC mice, which also displayed reduced NF-κB protein levels and F4/80+ macrophages trafficked to the lumbar DRGs following PAC treatment. In summary, our results are the first to demonstrate the biological role AEG-1, particularly in myeloid cells, in development of CIPN.

01 Jun 2025·Aquatic Toxicology

Temperature matters: Acute and latent toxicity of diluted bitumen to developing salmon is potentiated by a modest increase in water temperature

Article

Author: Edgar, Mackenzie ; Kennedy, Christopher J ; Lin, Feng ; Alderman, Sarah L ; Gillis, Todd E ; Çalık, Derin M ; Farrell, Anthony P

Heavy crude oil, like bitumen, is used globally for plastics, petrochemicals and road surfacing. Canada's oil sands are the world's third largest crude oil reserve, and diluted bitumen (dilbit) is transported across North America primarily via pipeline and rail. Two environmentally-relevant concentrations of dilbit were used with a suite of toxicological endpoints to determine if a 3 °C increase in ambient temperature (T_a) water modulated the effects of dilbit to coho salmon (Oncorhynchus kisutch) when exposed from fertilization to swim-up. The 10-20 % increase in mortality and 25 % reduction in hypoxia tolerance with dilbit exposure was magnified by 18 % and 40 %, respectively, in warmer water. Consequences of dilbit exposure persisted after 6 weeks of additional rearing in clean T_a water but were greatest in fish exposed to dilbit at elevated temperature: additional 20 % mortality and 30 % decrease in mass relative to controls, and a residual 20 % reduction in hypoxia tolerance not seen with dilbit exposure alone. Relatively lower induction of the Phase I biotransformation enzyme cyp1a and greater tissue PAC content in warm-exposed coho suggests reduced PAC metabolism as a mechanism for the observed potentiation. Thus, seasonal fluctuations and baseline increases in water temperature from climate change can exacerbate the adverse effects of oil spills on developing fish.

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PACC1

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