Last update 01 Nov 2024

GNB1L

Last update 01 Nov 2024

Basic Info

Synonyms

DGCRK3, G protein subunit beta 1 like, G protein subunit beta-like protein 1

+ [8]

Introduction-

Drugs associated with GNB1L

Leishmania multi-epitope vaccine(Shiraz University of Medical Sciences)

Target

GNB1L x LMLN

Mechanism

GNB1L modulators [+1]

Active Org.

Shiraz University of Medical Sciences

Originator Org.

Shiraz University of Medical Sciences

Active Indication

Leishmaniasis

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with GNB1L

100 Translational Medicine associated with GNB1L

0 Patents (Medical) associated with GNB1L

Literatures (Medical) associated with GNB1L

01 May 2024·Plant Disease

First Report of Fusarium falciforme Causing Root and Rhizome Rot of Epimedium sagittatum in China

Article

Author: Dan, Zhiwei ; Li, Diandian ; Wang, Xiaojie ; Dong, Chengming ; Hou, Wenchuan ; Chu, Leixia

Epimedium sagittatum (Sieb.et Zucc.) Maxim., a perennial herb, is an important medicinal plant, rich in flavonoids, and widely used in the treatment of sexual dysfunction, rheumatic disease, and cancers (Tan et al. 2016). In July 2022, a disease of root and rhizome was found on E. sagittatum aged 1-8 years in a planting area (266 ha) of Zhumadian City (32°58'12" N, 114°37'48" E), Henan Province, China. The disease incidence per field (660 m2) was around 10-15% in six randomly surveyed fields planted with about 10,000 E. sagittatum plants each. Symptoms included leaf yellowing, root and rhizome browning, rotting and necrosis, and eventually the whole plant wilted and died. Fifteen plants with symptoms were sampled to isolate the pathogen. Symptomatic tissues were cut into small pieces of 5×5 mm, surface sterilized with 75% ethanol for 30 s, followed by three rinses with sterile double-distilled water (ddH2O). The pieces were then surface disinfected with 0.1% HgCl2 for 30 s, rinsed three times with sterile ddH2O, placed onto potato dextrose agar (PDA) plates and incubated at 28°C in the dark for 5 days. Twelve deferent Fusarium spp. colonies were purified by excising hyphal tip onto PDA for cultivation. Pathogenicity test of all strains was performed. Only isolate GY2 could result in root and rhizome rot of host plant. Colonies of GY2 on PDA had abundant white aerial mycelia with yellow halo. Macroconidia were hyaline, falciform, with a slightly curved apical cell and blunt basal cell, 29.7~45.0 (average 38.3) × 4.5~6.6 (average 5.3) µm (n =50), with 2-3 septa. Microconidia were oval, or reniform, hyaline, 8.4~26.5 (average 16.5) × 2.7~6.0 (average 4.5) µm (n =50), with 0-2 septa. Morphological characteristics of isolate GY2 were consistent with those of the Fusarium solani species complex (FSSC) (Chehri et al. 2015). For molecular identification, a region of the translation elongation factor 1-α (TEF) and RNA polymerase second largest subunit (RPB2) of GY2 were PCR-amplified and sequenced using the primers EF1-728F/986R (Carbone et al. 1999) and RPB2-5f2/7cr (O'Donnell et al. 2010), respectively. The TEF and RPB2 sequences (GenBank accession nos. OR978135.1 and OR978136.1) of GY2 were concatenated for a phylogenetic analysis using the Bayesian method (Zhang et al. 2020). The phylogenetic tree revealed that isolate GY2 clustered with F. falciforme with a credibility value of 99%. Morphological and molecular results support identification of isolate GY2 as F. falciforme. A pathogenicity test was performed on 4-year-old healthy plants grown in pots. Twenty healthy plants were inoculated by pouring a 200 mL conidial suspension (1×106 conidia/mL) around the rhizome. Control plants received 200 mL of sterile ddH2O. All treatments were maintained in a greenhouse at 25±1°C and 80% relative humidity. The assay was conducted three times. After 20 days, similar symptoms as those in the field were observed on the inoculated plants, whereas controls remained asymptomatic. Fusarium falciforme was reisolated from the symptomatic plants and showed the same morphological and molecular characteristics as isolate GY2, fulfilling Koch’s postulates. Fusarium falciforme was reported to cause root rot of tobacco (Qiu et al. 2023) and industrial hemp (Paugh et al. 2022). However, this is the first report of F. falciforme causing root and rhizome rot of E. sagittatum. Our study will contribute to the development of strategies for the effective management of this disease on E. sagittatum.

01 Aug 2023·Molecular Cell

FACS-based genome-wide CRISPR screens define key regulators of DNA damage signaling pathways

Article

Author: Chen, Zhen ; Tang, Mengfan ; Su, Dan ; Feng, Xu ; Nie, Litong ; Huang, Min ; Yao, Fuwen ; Li, Siting ; Yin, Ling ; Zhang, Huimin ; Wang, Shimin ; Yu, Bin ; Wang, Chao ; Chen, Junjie ; Mou, Lisha ; Hart, Traver

DNA damage-activated signaling pathways are critical for coordinating multiple cellular processes, which must be tightly regulated to maintain genome stability. To provide a comprehensive and unbiased perspective of DNA damage response (DDR) signaling pathways, we performed 30 fluorescence-activated cell sorting (FACS)-based genome-wide CRISPR screens in human cell lines with antibodies recognizing distinct endogenous DNA damage signaling proteins to identify critical regulators involved in DDR. We discovered that proteasome-mediated processing is an early and prerequisite event for cells to trigger camptothecin- and etoposide-induced DDR signaling. Furthermore, we identified PRMT1 and PRMT5 as modulators that regulate ATM protein level. Moreover, we discovered that GNB1L is a key regulator of DDR signaling via its role as a co-chaperone specifically regulating PIKK proteins. Collectively, these screens offer a rich resource for further investigation of DDR, which may provide insight into strategies of targeting these DDR pathways to improve therapeutic outcomes.

01 Aug 2023·Molecular Cell

Genome-scale mapping of DNA damage suppressors through phenotypic CRISPR-Cas9 screens

Article

Author: Zhao, Yichao ; Jonkers, Jos ; Hoeg, Lisa ; Rubio Contreras, Diana ; Coté, Atina G ; Gómez Herreros, Fernando ; Lao, Linjiang ; Weile, Jochen ; Roth, Frederick P ; Gingras, Anne-Claude ; Kousholt, Arne Nedergaard ; Feng, Sumin ; Setiaputra, Dheva ; Lin, Zhen-Yuan ; Tabet, Daniel ; Melo, Henrique ; Durocher, Daniel

To maintain genome integrity, cells must accurately duplicate their genome and repair DNA lesions when they occur. To uncover genes that suppress DNA damage in human cells, we undertook flow-cytometry-based CRISPR-Cas9 screens that monitored DNA damage. We identified 160 genes whose mutation caused spontaneous DNA damage, a list enriched in essential genes, highlighting the importance of genomic integrity for cellular fitness. We also identified 227 genes whose mutation caused DNA damage in replication-perturbed cells. Among the genes characterized, we discovered that deoxyribose-phosphate aldolase DERA suppresses DNA damage caused by cytarabine (Ara-C) and that GNB1L, a gene implicated in 22q11.2 syndrome, promotes biogenesis of ATR and related phosphatidylinositol 3-kinase-related kinases (PIKKs). These results implicate defective PIKK biogenesis as a cause of some phenotypes associated with 22q11.2 syndrome. The phenotypic mapping of genes that suppress DNA damage therefore provides a rich resource to probe the cellular pathways that influence genome maintenance.

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GNB1L

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