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Last update 23 Jan 2025

NKRF

Last update 23 Jan 2025

Basic Info

Synonyms

ITBA4, NF-kappa-B-repressing factor, NF-kappaB repressing factor

+ [6]

Introduction

Enhances the ATPase activity of DHX15 by acting like a brace that tethers mobile sections of DHX15 together, stabilizing a functional conformation with high RNA affinity of DHX15 (PubMed:12381793). Involved in the constitutive silencing of the interferon beta promoter, independently of the virus-induced signals, and in the inhibition of the basal and cytokine-induced iNOS promoter activity (PubMed:12381793). Also involved in the regulation of IL-8 transcription (PubMed:12381793). May also act as a DNA-binding transcription regulator: interacts with a specific negative regulatory element (NRE) 5'-AATTCCTCTGA-3' to mediate transcriptional repression of certain NK-kappa-B responsive genes (PubMed:10562553).

Drugs associated with NKRF

Uroacitides

Target

NKRF

Mechanism

NF-kappa-B-repressing factor inhibitors

Active Org.

Hefei Everlife Pharmaceutical Co., Ltd.

Originator Org.

Hefei Lifeon Pharmaceutical Co., Ltd.

Active Indication

Breast Cancer [+2]

Inactive Indication-

Drug Highest PhaseApproved

First Approval Ctry. / Loc.

First Approval Date23 Jul 2004

Triolex

Target

ERK x NKRF

Mechanism

ERK inhibitors [+1]

Active Org.

NeurMedix, Inc. [+1]

Originator Org.

Harbor Diversified, Inc. [+1]

Active Indication

Alzheimer Disease [+6]

Inactive Indication

Amyotrophic Lateral Sclerosis [+18]

Drug Highest PhasePhase 3

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

Akt gene inhibitors(University of North Carolina)

Target

Akt x NKRF

Mechanism

AKT gene inhibitors [+1]

Active Org.

National Taiwan University Innovation & Incubation Co. Ltd. [+2]

Originator Org.-

Active Indication

Neoplasms

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

Clinical Trials associated with NKRF

NCT06757010

/ Not yet recruitingPhase 2

A Double-Blind, Randomized, Placebo-controlled, Study of NE3107 in Subjects with Early Parkinson's Disease

The goal of this clinical trial is to learn if bezisterim can treat movement symptoms of Parkinson's disease in patients that are 45 to 80 years old, in generally good physical and mental health, and are nearing the need for treatment to relieve their symptoms but have not yet been prescribed any form of levodopa or drug with similar activity. The main questions it aims to answer are:
* Will bezisterim decrease movement symptoms of Parkinson's disease?
* What medical problems do participants have when taking bezisterim?
Researchers will compare the effects of bezisterim treatment to placebo (a look-alike substance that contains no drug) to see if bezisterim works to treat movement symptoms of Parkinson's disease.
Participants will
* have a physical examination that includes an electrocardiogram
* take drug or placebo twice daily for four months
* visit a clinical site or receive an at home visit seven times over the course of five months

Start Date01 Feb 2025

Sponsor / Collaborator

BioVie, Inc.

NCT05970575

/ RecruitingPhase 2IIT

Open Label Phase IIa Study Evaluating the Safety and Efficacy of NE3107 in Improving Sleep and Fatigue in Subjects With Traumatic Brain Injury

This study seeks to measure changes in cognition through verbal and visual test procedures and changes in biomarkers of Traumatic Brain Injury and inflammatory and metabolic parameters.

Start Date21 Dec 2023

Sponsor / Collaborator

BioVie, Inc.

NCT05227820

/ CompletedPhase 2IIT

Anti-Inflammatory, Insulin-Sensitizing Agent for Treatment of Cognitive Decline Due to Degenerative Dementias

This study seeks to measure changes in cognition through verbal and visual test procedures and changes in biomarkers of Alzheimer's disease and inflammatory and metabolic parameters that can be measure in the central nervous system (CNS) with advanced neuroimaging techniques in patients treated with NE3107 (17a-ethynyl-androst-5-3b,7b,17b-triol).

Start Date19 Jan 2022

Sponsor / Collaborator

BioVie, Inc.

100 Clinical Results associated with NKRF

100 Translational Medicine associated with NKRF

0 Patents (Medical) associated with NKRF

554

Literatures (Medical) associated with NKRF

01 Feb 2025·European Journal of Pharmacology

NRF-mediated autophagy and UPR: Exploring new avenues to overcome cancer chemo-resistance

Review

Author: Ghavami, Saeid ; Shafiee, Sayed Mohammad ; Ashtari, Niloufar ; Nasery, Mahshid Moballegh ; Siri, Morvarid ; Tabasi, Farhad ; Kokabi, Fariba ; Saffari-Chaleshtori, Javad ; Igder, Somayeh ; Mokarram, Pooneh ; Dastghaib, Sanaz ; Zamani, Mozhdeh ; Ramezani, Fatemeh ; Mostafavi-Pour, Zohreh ; Vakili, Omid ; Wiechec, Emilia ; Niknam, Maryam

The development of chemo-resistance remains a significant hurdle in effective cancer therapy. NRF1 and NRF2, key regulators of redox homeostasis, play crucial roles in the cellular response to oxidative stress, with implications for both tumor growth and resistance to chemotherapy. This study delves into the dualistic role of NRF2, exploring its protective functions in normal cells and its paradoxical support of tumor survival and drug resistance in cancerous cells. We investigate the interplay between the PERK/NRF signaling pathway, ER stress, autophagy, and the unfolded protein response, offering a mechanistic perspective on how these processes contribute to chemoresistance. Our findings suggest that targeting NRF signaling pathways may offer new avenues for overcoming resistance to chemotherapeutic agents, highlighting the importance of a nuanced approach to redox regulation in cancer treatment. This research provides a molecular basis for the development of NRF-targeted therapies, potentially enhancing the efficacy of existing cancer treatments and offering hope for more effective management of resistant tumors.

01 Jan 2025·Comparative Biochemistry and Physiology Part C: Toxicology & Pharmacology

Time-restricted feeding modulates gene expression related with rhythm and inflammation in Mongolian gerbils

Article

Author: Wang, Xi-Zhi ; Wang, Zhen-Shan ; Wang, Chen-Zhu ; Zhang, Xue-Ying ; Yang, Lin ; Wang, De-Hua

Time-restricted feeding (TRF) has the potential to modulate circadian rhythm and widely studied in humans and laboratory mice. However, less is known about the physiological responses to TRF in wild mammals. Here, we used Mongolian gerbils, Meriones unguiculatus, to explore the effect of 6-week TRF on gene expression related with circadian rhythm and inflammation. The TRF gerbils had higher cumulative food intake than the ad libitum (AL) group, but body mass, feeding frequency/time and metabolic rate did not differ between groups. In the hypothalamus, downregulation of rhythm-related genes Per3, Cry1 and Dbp was detected in the daytime-restricted feeding (DRF) group and Cry1 was downregulated in the nighttime-restricted feeding (NRF) group. In the liver, the expression of Per1/3, Rev-erbα/β and Dbp was lower, and Bmal1 was higher in the DRF than in AL group, while NRF gerbils showed no changes. In the colon, the expression of Bmal1 and Cry1 was higher but Per3, Rev-erbα/β and Dbp were lower in the DRF than in AL group. Further, the expression of inflammation-related genes such as NF-κB, IL-1β, IL-18 and Nlrp3 was lower in the liver of DRF gerbils, and IL-1β was lower both in the hypothalamus and liver of NRF gerbils. Moreover, the genes related with inflammation such as NF-κB, Nlrp3, IL-10/18/1β and Tnf-α were positively or negatively correlated with multiple rhythm-related genes in the central and peripheral organs. In conclusion, TRF, particularly DRF, could modulate rhythm-related genes in the central and peripheral tissues and reduce hepatic expression of inflammation-related genes in gerbils.

31 Dec 2024·Epigenetics

TET1 inhibits the migration and invasion of cervical cancer cells by regulating autophagy

Article

Author: Ren, Ji ; Ding, Yan ; Tan, Yujie ; Zan, Yuxin ; Chen, Xiuying ; Wang, Shan ; Li, Jing

Methylation modifications play pertinent roles in regulating gene expression and various biological processes. The silencing of the demethylase enzyme TET1 can affect the expressions of key oncogenes or tumour suppressor genes, thus contributing to tumour formation. Nonetheless, how TET1 affects the progression of cervical cancer is yet to be elucidated. In this study, we found that the expression of TET1 was significantly downregulated in cervical cancer tissues. Functionally, TET1 knockdown in cervical cancer cells can promote cell proliferation, migration, invasion, cervical xenograft tumour formation and EMT. On the contrary, its overexpression can reverse the aforementioned processes. Moreover, the autophagy level of cervical cancer cells can be enhanced after TET1 knockdown. Mechanistically, methylated DNA immunoprecipitation (MeDIP)-sequencing and MeDIP quantitative real-time PCR revealed that TET1 mediates the methylation of autophagy promoter regions. These findings suggest that TET1 affects the autophagy of cervical cancer cells by altering the methylation levels of NKRF or HIST1H2AK, but the specific mechanism needs to be investigated further.

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