Last update 01 Nov 2024

RAD52

Last update 01 Nov 2024

Basic Info

Synonyms

DNA repair protein RAD52 homolog, RAD52, RAD52 homolog, DNA repair protein

Introduction

Involved in double-stranded break repair. Plays a central role in genetic recombination and DNA repair by promoting the annealing of complementary single-stranded DNA and by stimulation of the RAD51 recombinase.

Drugs associated with RAD52

C791-0064

Target

RAD52

Mechanism

RAD52 inhibitors

Active Org.

Chengdu University

Originator Org.

Chengdu University

Active Indication

Neoplasms

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

D-I03

Target

RAD52

Mechanism

RAD52 modulators

Active Org.

Drexel University College of Medicine

Originator Org.

Drexel University College of Medicine

Active Indication

Neoplasms

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

6-OH-dopa

Target

RAD52

Mechanism

RAD52 inhibitors

Active Org.

Temple University Graduate School

Originator Org.

Temple University Graduate School

Active Indication

Neoplasms

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with RAD52

100 Translational Medicine associated with RAD52

0 Patents (Medical) associated with RAD52

1,508

Literatures (Medical) associated with RAD52

01 Dec 2024·Experimental Parasitology

RAD51 recombinase and its paralogs: Orchestrating homologous recombination and unforeseen functions in protozoan parasites

Article

Author: Sosa-Mondragon, Sharon Itzel ; Flores-Vega, Jose Jesus ; Puente-Rivera, Jonathan ; Camacho-Nuez, Minerva ; Sosa-Mondragón, Sharon Itzel ; Alvarez-Sánchez, María Elizbeth ; Flores-Vega, Jose Jesús

The DNA of protozoan parasites is highly susceptible to damage, either induced by environmental agents or spontaneously generated during cellular metabolism through reactive oxygen species (ROS). Certain phases of the cell cycle, such as meiotic recombination, and external factors like ionizing radiation (IR), ultraviolet light (UV), or chemical genotoxic agents further increase this susceptibility. Among the various types of DNA damage, double-stranded breaks (DSBs) are the most critical, as they are challenging to repair and can result in genetic instability or cell death. DSBs caused by environmental stressors are primarily repaired via one of two major pathways: non-homologous end joining (NHEJ) or homologous recombination (HR). In multicellular eukaryotes, NHEJ predominates, but in unicellular eukaryotes such as protozoan parasites, HR seems to be the principal mechanism for DSB repair. The HR pathway is orchestrated by proteins from the RAD52 epistasis group, including RAD51, RAD52, RAD54, RAD55, and the MRN complex. This review focuses on elucidating the diverse roles and significance of RAD51 recombinase and its paralogs in protozoan parasites, such as Acanthamoeba castellanii, Entamoeba histolytica (Amoebozoa), apicomplexan parasites (Chromalveolata), Naegleria fowleri, Giardia spp., Trichomonas vaginalis, and trypanosomatids (Excavata), where they primarily function in HR. Additionally, we analyze the diversity of proteins involved in HR, both upstream and downstream of RAD51, and discuss the implications of these processes in parasitic protozoa.

01 Nov 2024·European Journal of Medicinal Chemistry

An update on small molecule compounds targeting synthetic lethality for cancer therapy

Review

Author: Wang, Chengdi ; Liu, Jie ; Zhang, Jifa ; Ren, Yijiu ; Wu, Defa ; Zhang, Yiwen ; Li, Yang ; Luo, Jiaxiang

Targeting cancer-specific vulnerabilities through synthetic lethality (SL) is an emerging paradigm in precision oncology. A SL strategy based on PARP inhibitors has demonstrated clinical efficacy. Advances in DNA damage response (DDR) uncover novel SL gene pairs. Beyond BRCA-PARP, emerging SL targets like ATR, ATM, DNA-PK, CHK1, WEE1, CDK12, RAD51, and RAD52 show clinical promise. Selective and bioavailable small molecule inhibitors have been developed to induce SL, but optimization for potency, specificity, and drug-like properties remains challenging. This article illuminated recent progress in the field of medicinal chemistry centered on the rational design of agents capable of eliciting SL specifically in neoplastic cells. It is envisioned that innovative strategies harnessing SL for small molecule design may unlock novel prospects for targeted cancer therapeutics going forward.

09 Sep 2024·Genes to cells : devoted to molecular & cellular mechanisms

RNA-DNA hybrids on protein coding genes are stabilized by loss of RNase H and are associated with DNA damages during S-phase in fission yeast.

Article

Author: Sagi, Tomoko ; Sadato, Daichi ; Kanoh, Yutaka ; Sasanuma, Hiroyuki ; Takayasu, Kazuto ; Masai, Hisao

RNA-DNA hybrid is a part of the R-loop which is an important non-standard nucleic acid structure. RNA-DNA hybrid/R-loop causes genomic instability by inducing DNA damages or inhibiting DNA replication. It also plays biologically important roles in regulation of transcription, replication, recombination and repair. Here, we have employed catalytically inactive human RNase H1 mutant (D145N) to visualize RNA-DNA hybrids and map their genomic locations in fission yeast cells. The RNA-DNA hybrids appear as multiple nuclear foci in rnh1∆rnh201∆ cells lacking cellular RNase H activity, but not in the wild-type. The majority of RNA-DNA hybrid loci are detected at the protein coding regions and tRNA. In rnh1∆rnh201∆ cells, cells with multiple Rad52 foci increase during S-phase and about 20% of the RNA-DNA hybrids overlap with Rad52 loci. During S-phase, more robust association of Rad52 with RNA-DNA hybrids was observed in the protein coding region than in M-phase. These results suggest that persistent RNA-DNA hybrids in the protein coding region in rnh1∆rnh201∆ cells generate DNA damages during S-phase, potentially through collision with DNA replication forks.

News (Medical) associated with RAD52

23 Nov 2022

·www.biospace.com

Rain Therapeutics Announces a Poster Presentation at the 2022 San Antonio Breast Cancer Symposium

NEWARK, Calif., Nov. 23, 2022 (GLOBE NEWSWIRE) -- Rain Therapeutics Inc. (NasdaqGS: RAIN), (Rain), a late-stage biotechnology company developing precision oncology therapeutics with a lead product candidate, milademetan, an oral, small molecule inhibitor of the MDM2-p53 complex that reactivates p53, today announced a poster presentation at the upcoming 2022 San Antonio Breast Cancer Symposium (SABCS) taking place on December 6-10, 2022 in San Antonio, TX. Presentation Title: Genetic alterations in breast cancer associated with MDM2 dependency and sensitivity to the MDM2 inhibitor milademetan Authors: Francois-Clement Bidard, Diana Bello Roufai, Arielle J. Medford, Vijaya Tirunagaru, Robert C. Doebele, Aditya Bardia Poster Session / Category: Session 6 / Treatment: Therapeutic Strategies – Novel Targets and Targeted Agents Poster Number: P6-10-10 Session Date and Time: Friday, December 9, 2022; 7:00 AM CT Location: Henry B. Gonzalez Convention Center, Hall 1 A copy of the presentation materials can be accessed by visiting the "Resources” section of the Rain website after the conclusion of the presentation and will be archived on the Rain website. About Rain Therapeutics Inc. Rain Therapeutics Inc. is a late-stage precision oncology company developing therapies that target oncogenic drivers to genetically select patients it believes will most likely benefit. This approach includes using a tumor-agnostic strategy to select patients based on their tumors’ underlying genetics rather than histology. Rain’s lead product candidate, milademetan, is a small molecule, oral inhibitor of MDM2-p53 complex that reactivates p53. In addition to milademetan, Rain is also developing a preclinical program that is focused on inducing synthetic lethality in cancer cells by inhibiting RAD52. Investor Contact Dan Ferry LifeSci Advisors +1.617.430.7576 daniel@lifesciadvisors.com Media Contact Jordyn Temperato LifeSci Communications jtemperato@lifescicomms.com

18 Nov 2022

·www.globenewswire.com

Rain Therapeutics to Participate in Piper Sandler’s 34th Annual Healthcare Conference

NEWARK, Calif., Nov. 18, 2022 (GLOBE NEWSWIRE) -- Rain Therapeutics Inc. (NasdaqGS: RAIN), (“Rain”), a late-stage biotechnology company developing precision oncology therapeutics with a lead product candidate, milademetan, an oral, small molecule inhibitor of the MDM2-p53 complex that reactivates p53, today announced that it will be participating in Piper Sandler’s 34th Annual Healthcare Conference, being held November 29 – December 1, 2022, in New York. Avanish Vellanki, chief executive officer of Rain, will be participating in a fireside chat on Thursday, December 1 at 1:30 p.m. ET. A webcast of the fireside chat can be accessed here. The Company’s management team will participate in one-on-one investor meetings. To request a meeting, please contact your Piper Sandler representative. About Rain Therapeutics Inc. Rain Therapeutics Inc. is a late-stage precision oncology company developing therapies that target oncogenic drivers for which it is able to genetically select patients it believes will most likely benefit. This approach includes using a tumor-agnostic strategy to select patients based on their tumors’ underlying genetics rather than histology. Rain’s lead product candidate, milademetan, is a small molecule, oral inhibitor of MDM2-p53 complex that reactivates p53. In addition to milademetan, Rain is also developing a preclinical program that is focused on inducing synthetic lethality in cancer cells by inhibiting RAD52. Investor ContactDan FerryLifeSci Advisors+1.617.430.7576daniel@lifesciadvisors.com Media Contact Jordyn Temperato LifeSci Communications jtemperato@lifescicomms.com

17 Nov 2022

·www.globenewswire.com

Rain Therapeutics Announces an Oral Presentation at the Connective Tissue Oncology Society Annual Meeting

NEWARK, Calif., Nov. 17, 2022 (GLOBE NEWSWIRE) -- Rain Therapeutics Inc. (NasdaqGS: RAIN), (Rain), a late-stage biotechnology company developing precision oncology therapeutics with a lead product candidate, milademetan, an oral, small molecule inhibitor of the MDM2-p53 complex that reactivates p53, today announced an oral presentation at the Connective Tissue Oncology Society (CTOS) Annual Meeting taking place on November 16-19, 2022 in Vancouver, BC, Canada. Presentation Title: Sustained disease control with MDM2 inhibitor milademetan in patients with advanced dedifferentiated liposarcomaSession:Session 3: Medical & Pediatric Oncology and Clinical Trials Presenter:Mrinal M. Gounder, M.D., Associate Attending Physician Memorial Sloan Kettering Cancer Center and Weill Cornall Medical Center, New York, NY, USASession Date and Time:Thursday, November 17, 2022; 1:00-2:30 pm Pacific TimeLocation:VCC: East Exhibition Hall B A copy of the presentation materials can be accessed by visiting the "Resources” section of the Rain website after the conclusion of the presentation and will be archived on the Rain website. About Rain Therapeutics Inc.Rain Therapeutics Inc. is a late-stage precision oncology company developing therapies that target oncogenic drivers to genetically select patients it believes will most likely benefit. This approach includes using a tumor-agnostic strategy to select patients based on their tumors’ underlying genetics rather than histology. Rain’s lead product candidate, milademetan, is a small molecule, oral inhibitor of MDM2-p53 complex that reactivates p53. In addition to milademetan, Rain is also developing a preclinical program that is focused on inducing synthetic lethality in cancer cells by inhibiting RAD52. Investor ContactDan FerryLifeSci Advisors+1.617.430.7576daniel@lifesciadvisors.com Media Contact Jordyn Temperato LifeSci Communications jtemperato@lifescicomms.com

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RAD52

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