SLC33A1

Last update 08 May 2025

Basic Info

Synonyms

ACATN, Acetyl-CoA transporter 1, acetyl-Coenzyme A transporter

+ [8]

Introduction

Acetyl-CoA transporter that mediates active acetyl-CoA import through the endoplasmic reticulum (ER) membrane into the ER lumen where specific ER-based acetyl-CoA:lysine acetyltransferases are responsible for the acetylation of ER-based protein substrates, such as BACE1 (PubMed:20826464, PubMed:24828632). Necessary for O-acetylation of gangliosides (PubMed:9096318).

100 Clinical Results associated with SLC33A1

100 Translational Medicine associated with SLC33A1

0 Patents (Medical) associated with SLC33A1

2,865

Literatures (Medical) associated with SLC33A1

01 Jul 2025·Cellular Signalling

Function of intramitochondrial melatonin and its association with Warburg metabolism

Review

Author: Fan, Lihong ; Bai, Yidong ; Sharma, Ramaswamy ; Chuffa, Luiz Gustavo de Almeida ; Loh, Doris ; Reiter, Russel J ; Cardinali, Daniel P

Warburg metabolism (aerobic glycolysis) is accompanied by high mitochondrial reactive oxygen species (ROS) generation from the electron transport chain; this is a "Hallmark of Cancer". The elevated ROS sustain the growth and proliferation of the cancer cells. Melatonin is a potent and functionally diverse free radical scavenger and antioxidant that is synthesized in the mitochondria of non-pathological cells and normally aids in keeping mitochondrial ROS levels low and in maintaining redox homeostasis. Because the glucose metabolite, pyruvate, does not enter mitochondria of Warburg metabolizing cells due to the inhibition of pyruvate dehydrogenase complex (PDH), acetyl coenzyme A production is diminished. Acetyl coenzyme A is a necessary co-substrate with serotonin for melatonin synthesis; thus, intramitochondrial melatonin levels become reduced in cancer cells. The hypothesis is that the depressed melatonin levels initiate aerobic glycolysis and allow the exaggerated ROS concentrations to go uncontested; the authors speculate that the elevated mtROS upregulates hypoxia inducible factor 1α (HIF-1α)/pyruvate dehydrogenase kinase (PDK) axis which inhibits PDH, thereby supporting cancer cell proliferation and stimulating cancer biomass. Exposing Warburg metabolizing cancer cells to melatonin elevates intramitochondrial melatonin, thereby reducing mtROS and concurrently interrupting aerobic glycolysis and inhibiting tumor cell proliferation. Mechanistically, higher mitochondrial melatonin levels by supplementation directly upregulates the sirtuin 3 (SIRT3)/FOXO/PDH axis, allowing pyruvate entry into mitochondria and enhancing intrinsic mitochondrial melatonin production as in non-pathological cells. Additionally, melatonin inhibits HIF1α, thereby decreasing PDK activity and disinhibiting PDH, so pyruvate enters mitochondria and is metabolized to acetyl coenzyme A, resulting in reversal of Warburg metabolism.

01 Jun 2025·Journal of Pharmaceutical Sciences

Progressive amyloid-β accumulation in the brain leads to altered protein expressions in the liver and kidneys of APP knock-in mice

Article

Author: Saito, Takashi ; Iwata, Yumi ; Yagi, Ryotaro ; Masuda, Takeshi ; Uemura, Tatsuki ; Kaneko, Yui ; Ogata, Seiryo ; Ito, Shingo ; Otsuka, Mitsumi ; Ohtsuki, Sumio ; Saido, Takaomi

Impaired hepatic and renal function influence Alzheimer's disease (AD) progression; however, whether AD progression affects these important organ functions remains unclear. Here, we investigated the impact of AD progression, characterized by brain amyloid-beta (Aβ) accumulation, on liver and kidney function of App^{NL-G-F/NL-G-F} (APP-KI) mice using quantitative proteomics. SWATH-based quantitative proteomics revealed changes in mitochondrial, drug metabolism, and pharmacokinetic-related proteins in mouse liver and kidneys during the early (2-month-old) and intermediate (5-month-old) stages of Aβ accumulation. Notably, in 5-month-old APP-KI mouse liver, 25 phase I/II metabolizing enzymes (8 CYPs, 7 UGTs, 7 CESs, and 3 SLCs) and five transporters (2 ABCs and 3 SLCs) were significantly altered; specifically, Ugt1a9 and Slc33a1 protein abundances increased, whereas Ugt1a1 and Abcc3 protein abundances decreased. In the kidneys, 13 phase I/II metabolizing enzymes and 10 ABC-SLC transporters were altered, including Ugt1a6, Ugt1a7, Slc22a7, and Abcb1a. Additionally, plasma proteins, such as albumin and alpha-1-acid glycoprotein, which are critical for drug binding and distribution, were also altered. These results underscore the significant role of progressive brain Aβ accumulation in modifying hepatic and renal protein abundances, potentially influencing drug metabolism and disposition in AD. Our findings provide novel insights into the complex relationship between AD progression and organ dysfunction.

01 May 2025·The Journal of Pain

Angiotensin II type 1 receptor activation induces dorsal horn capillary constriction and pain hypersensitivity

Article

Author: Bates, David O ; McTernan, Philip G ; Hardowar, Lydia D ; Hulse, Richard P ; Sheavyn, Matthew

Vascular disturbance is a key factor in the development of neurological disease, with reduced integrity of the capillary network in the dorsal horn implicated in activation of nociceptive neural circuits and induction of pain states. Pericytes regulate capillary health and tone, with pericyte dysfunction in cerebral tissue associated with neurodegenerative disorders. Our work demonstrates that spinal cord nociceptive processing is influenced by angiotensin II type 1 (AT1) receptor mediated capillary constriction. Intravital imaging of the mouse spinal cord demonstrated angiotensin II induced cessation of spinal cord capillary perfusion. Intrathecal administration of angiotensin II induced narrowing of capillary diameter, which was accompanied by mechanical allodynia and heat hyperalgesia in adult male and female mice. Angiotensin II mediated reduction of spinal cord blood flow and pericyte activation, was prevented by AT1 receptor inhibition via losartan treatment. Losartan prevented angiotensin II induced pain. Integrity of dorsal horn capillary endothelium was protected by co-treatment with losartan preventing angiotensin II induced loss of CD31 immunoreactivity. This investigation demonstrates that AT1 regulates the dorsal horn capillary network and is fundamental in modulating nociceptive processing and perception of pain. Here we identify a novel cellular and mechanistic target for the induction of pain hypersensitivity. PERSPECTIVE: Intrathecally delivered Angiotensin II induced mechanical and heat hypersensitivity in male and female mice. Capillary constriction in the dorsal horn was induced by Angiotensin II treatment and led to degeneration of the endothelium. Angiotensin II induced pericyte activation was Angiotensin II type 1 receptor dependent.

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SLC33A1

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