Last update 01 Nov 2024

PCLAF

Last update 01 Nov 2024

Basic Info

Synonyms

HCV NS5A-transactivated protein 9, Hepatitis C virus NS5A-transactivated protein 9, KIAA0101

+ [12]

Introduction

PCNA-binding protein that acts as a regulator of DNA repair during DNA replication. Following DNA damage, the interaction with PCNA is disrupted, facilitating the interaction between monoubiquitinated PCNA and the translesion DNA synthesis DNA polymerase eta (POLH) at stalled replisomes, facilitating the bypass of replication-fork-blocking lesions. Also acts as a regulator of centrosome number.

Drugs associated with PCLAF

SM-1044

Target

PCLAF

Mechanism

PCLAF modulators

Active Org.

Guizhou Medical University

Originator Org.

Guizhou Medical University

Active Indication

Neoplasms

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

AD-4

Target

PCLAF

Mechanism

PCLAF modulators

Active Org.

Guizhou Medical University

Originator Org.

Guizhou Medical University

Active Indication

Neoplasms

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

CN118291393

Patent Mining

Target

PCLAF

Mechanism-

Active Org.

Xiangya Hospital Central South University

Originator Org.

Xiangya Hospital Central South University

Active Indication

Nutritional and Metabolic Diseases

Inactive Indication-

Drug Highest PhaseDiscovery

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with PCLAF

100 Translational Medicine associated with PCLAF

0 Patents (Medical) associated with PCLAF

8,147

Literatures (Medical) associated with PCLAF

01 Jan 2025·Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids

Re-evaluation of the canonical PAF pathway in cutaneous anaphylaxis

Article

Author: Yanagida, Keisuke ; Murakami, Makoto ; Shimizu, Takao ; Nagase, Takahide ; Suzuki, Tomoyuki ; Shindou, Hideo ; Yoshida-Hashidate, Tomomi ; Taketomi, Yoshitaka

Platelet-activating factor (PAF) is a potent classical lipid mediator that plays a critical role in various diseases such as allergy and nervous system disorders. In the realm of allergy, previous studies suggested that PAF is generated in response to extracellular stimuli and contributes to allergic reactions via PAF receptor (PAFR). However, the sources of endogenous PAF and its pathophysiological dynamics remain largely elusive in vivo. Here, we report that rapid and local PAF generation completely depends on lysophospholipid acyltransferase 9 (LPLAT9, also known as LPCAT2) expressed in mast cells in IgE-mediated passive cutaneous anaphylaxis. However, we found that LPLAT9 knockout (KO) mice did not display attenuated vascular leakage. Additionally, decreased vascular leakage was observed in PAFR KO mice, but not in endothelial cell-specific mice in this model. These divergences highlight a yet unsolved complexity of the biological functions of PAF and PAFR in a pathophysiological process.

31 Dec 2024·BioengineeredQ4 · BIOLOGY

The role of second generation sequencing technology and nanomedicine in the monitoring and treatment of lower extremity deep vein thrombosis susceptibility genes

Q4 · BIOLOGY

ArticleOA

Author: Wu, Jinchun ; Li, Wenhui ; Wang, Chunsheng ; Chang, Rong ; Kong, Xiangqi

Rong Chang, Chunsheng Wang, Xiangqi Kong, Wenhui Li and Jinchun Wu. The role of second generation sequencing technology and nanomedicine in the monitoring and treatment of lower extremity deep vein thrombosis susceptibility genes. Bioengineered. 2021 Nov. doi: 10.1080/21655979.2021.2003926.Since publication, significant concerns have been raised about the compliance with ethical policies for human research and the integrity of the data reported in the article.When approached for an explanation, the authors provided some original data but were not able to provide all the necessary supporting information. As verifying the validity of published work is core to the scholarly record's integrity, we are retracting the article. All authors listed in this publication have been informed.We have been informed in our decision-making by our editorial policies and the COPE guidelines.The retracted article will remain online to maintain the scholarly record, but it will be digitally watermarked on each page as 'Retracted.'

01 Oct 2024·Journal of Leukocyte Biology

Evidence that keratinocyte microvesicle particles carrying platelet-activating factor mediate the widespread multiorgan damage associated with intoxicated thermal burn injury

Article

Author: Thyagarajan, Anita ; Lohade, Rushabh P ; Zhang, Wenfeng ; Manjrekar, Pranali ; Sabit, Taskin ; Travers, Jeffrey B ; Rapp, Christine M ; Henkels, Karen M ; Singh, Shikshita ; Brewer, Chad ; Sahu, Ravi P

AbstractThermal burn injuries can result in significant morbidity and mortality. The combination of ethanol intoxication with thermal burn injury results in increased morbidity through an exaggerated inflammatory response involving many organs. Recent studies have linked involvement of the lipid mediator platelet-activating factor (PAF) in the pathology associated with intoxicated thermal burn injury (ITBI). The present studies tested the roles of PAF and the elevated levels of subcellular microvesicle particles (MVP) generated in response to ITBI in the subsequent multiorgan toxicity. First, thermal burn injury of HaCaT keratinocytes preincubated with ethanol resulted in augmented MVP release, which was blocked by inhibiting the PAF-generating enzyme cytosolic phospholipase A2 and the PAF receptor (PAFR). Second, ITBI of mice resulted in increased proinflammatory cytokine production and neutrophilic inflammation in multiple organs, which were not present in mice deficient in PAFRs or the MVP-generating enzyme acid sphingomyelinase (aSMase). Moreover, the increased bacterial translocation from the gut to mesenteric lymph nodes previously reported in murine ITBI was also dependent on PAFR and aSMase. MVP released from ITBI-treated keratinocytes contained high levels of PAFR agonistic activity. Finally, use of topical aSMase inhibitor imipramine following ITBI attenuated the widespread organ inflammatory response of ITBI, suggesting a potential therapeutic for this condition. These studies provide evidence for PAF-enriched MVP generated in skin, which then act on the gut PAFR, resulting in bacterial translocation as the mechanism for the multiorgan dysfunction associated with ITBI. Inasmuch as aSMase inhibitors are widely available, these studies could result in effective treatments for ITBI.

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PCLAF

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