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Last update 08 May 2025

PFKL

Last update 08 May 2025

Basic Info

Synonyms

6-phosphofructokinase type B, ATP-dependent 6-phosphofructokinase, liver type, ATP-PFK

+ [6]

Introduction

Catalyzes the phosphorylation of D-fructose 6-phosphate to fructose 1,6-bisphosphate by ATP, the first committing step of glycolysis (PubMed:22923583). Negatively regulates the phagocyte oxidative burst in response to bacterial infection by controlling cellular NADPH biosynthesis and NADPH oxidase-derived reactive oxygen species. Upon macrophage activation, drives the metabolic switch toward glycolysis, thus preventing glucose turnover that produces NADPH via pentose phosphate pathway (By similarity).

Drugs associated with PFKL

WO2025082533

Patent Mining

Target

PFKL

Mechanism-

Active Org.

Shanghai Ennovabio Pharmaceuticals Co. Ltd.

Originator Org.

Shanghai Ennovabio Pharmaceuticals Co. Ltd.

Active Indication

Autoimmune Diseases [+9]

Inactive Indication-

Drug Highest PhaseDiscovery

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with PFKL

100 Translational Medicine associated with PFKL

0 Patents (Medical) associated with PFKL

222

Literatures (Medical) associated with PFKL

01 May 2025·Pharmacological Research

Cardiac PDK4 promotes neutrophilic PFKL methylation and drives the innate immune response in diabetic myocardial infarction

Article

Author: Chen, Lang ; Yan, Longxin ; Su, Gaijuan ; Liu, Lihong ; Yang, Long ; Gong, Lili ; Yang, Song

NETosis plays a pivotal role in the innate immune response after diabetic myocardial infarction (MI), exerting a profound influence on the overall pathological process and potential recovery outcomes. The metabolism of diabetic cardiomyocyte actively creates a specialized micro environment for the innate immune response after MI. However, the mechanism by which cardiac metabolism drives NETosis remains unclear. Utilizing public databases of human MI sc-RNA datasets, we discovered that cardiomyocyte PDK4 expression mediates the intensification of glycolysis, which is strongly correlated with NETosis. Through mass spectrometry imaging and phenotype assessment, we ascertained that specific knockout of PDK4 in cardiomyocytes (PDK4^fl/flMyh6^Cre, male, 6 weeks) led to a reduction in NETosis by restraining micro environmental lactate (LA) production. In addition, the role of LA in promoting NETosis has been further corroborated by in vivo/in vitro experiments involving LA supplementation and its absence. Moreover, LA redirects neutrophil metabolic flux from glycolysis to the pentose-phosphate pathway (PPP). Mechanistically, LA triggers metabolic remodeling through the PRMT9-mediated methylation of PFKL at the R301 residue, resulting in PFKL inactivation and the consequent restriction of glycolysis. Our findings reveal the crucial role of cardiomyocyte metabolism in NETosis, shedding light on the role of LA as a vital signaling molecule in the crosstalk between cardiomyocytes and neutrophils. Importantly, we screened pitavastatin, a potential inhibitor of PDK4 among the FDA-approved drugs, and verified that it can alleviate NETosis in diabetic MI, which provides a rationale for drug selection in diabetic MI patients.

04 Feb 2025·ACS Nano

Lanthanide Metal–Organic Framework Flowers for Proteome Profiling and Biomarker Identification in Ultratrace Biofluid Samples

Article

Author: Xu, Zhixiao ; Chen, Youming ; Shen, Guangxia ; Ding, Xianting ; Wang, Aiting ; Jiang, Lai ; Zhang, Shuang

Identifying effective biomarkers has long been a persistent need for early diagnosis and targeted therapy of disease. While mass spectrometry-based label-free proteomics with trace cell has been demonstrated, deep proteomics with ultratrace human biofluid remains challenging due to low protein concentration, extremely limited patient sample volume, and substantial protein contact losses during preprocessing. Herein, we proposed and validated lanthanide metal-organic framework flowers (MOF-flowers), as effective materials, to trap and enrich protein in biofluid jointly through cation-π interaction and O-Ln coordination. We further developed a MOF-flower assisted simplified and single-pot Sample Preparation (Mass-SP) workflow that incorporates protein capture, digest, and peptide elute into one single PCR tube to maximally avoid adsorptive sample loss. We adopted Mass-SP to decipher aqueous humor (AH) proteome signatures from cataract and retinal vein occlusion (RVO) patients and quantified ∼3900 proteins in merely 1 μL of AH. Combined with machine learning, we further identified PFKL as a prioritization biomarker for RVO disease with the areas under the curves of 0.95 ± 0.04. Mass-SP presents a strategy to identify de novo biomarkers and explore potential therapeutic targets with extremely limited clinical human body fluid resources.

01 Feb 2025·Acta Biochimica et Biophysica Sinica

Alpha-lipoic acid targets <italic>KLF7</italic> expression to inhibit cervical cancer progression

Article

Author: Li, Hongtao ; Xu, Gang ; Tian, Jiazhen ; Chen, Yuechan ; Mao, Yi ; Zhang, Zhiwei

It is unclear what part KLF7 plays in cervical cancer. In this study, immunohistochemical and bioinformatics analyses reveal that KLF7 expression is lower in normal cervical tissues than in cervical cancer tissues, and the high level of KLF7 transcripts in cervical cancer tissues is negatively correlated with patients' overall and disease-free survival. In addition, KLF7 overexpression facilitates the proliferation, migration, and invasion of cervical cells, reduces PFKL expression, and increases the expressions of KLF4, Nanog, OCT4, CD44, SOX2, and ACADL. Additionally, knocking out the Exon 2 of KLF7 in HeLa cells results in a decrease in the total expression of KLF7 but an increase in the nuclear expression of KLF7, an increase in the capacity for proliferation, migration, invasion, and oncogenicity, and an increase in the density and ridge density of mitochondria. Consistent with these findings, RNA-seq analysis shows that knocking out the Exon 2 of KLF7 facilitates the expression of gene sets associated with cancer compared with that in wild-type HeLa cells. Moreover, the administration of alpha-lipoic acid (ALA) leads to a reduction in KLF7 expression in cells and tumor tissues, a suppression of the proliferation, migration, and invasion of HeLa and SiHa cells, and an increase in the carcinogenic potential of HeLa cells, while KLF7 overexpression shows the opposite effect on the expressions of ACADL and PFKL in HeLa and SiHa cells. In conclusion, KLF7 promotes the development of cervical cancer, and ALA can downregulate KLF7 expression and play a positive role in cervical cancer treatment.

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PFKL

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