更新于：2024-11-01

CBX1

更新于：2024-11-01

基本信息

别名

CBX、CBX1、chromobox 1

+ [11]

简介

Component of heterochromatin. Recognizes and binds histone H3 tails methylated at 'Lys-9', leading to epigenetic repression. Interaction with lamin B receptor (LBR) can contribute to the association of the heterochromatin with the inner nuclear membrane.

关联

项与 CBX1 相关的药物

UNC7047

靶点

CBX1 x CBX3 x CBX5

作用机制

CBX1 inhibitors [+2]

在研机构

The University of North Carolina at Chapel Hill

原研机构

The University of North Carolina at Chapel Hill

在研适应症

诊断试剂

非在研适应症-

最高研发阶段临床前

首次获批国家/地区-

首次获批日期1800-01-20

UNC-7565

靶点

CBX1 x CBX3 x CBX5

作用机制

CBX1 inhibitors [+2]

在研机构

The University of North Carolina at Chapel Hill

原研机构

The University of North Carolina at Chapel Hill

在研适应症

诊断试剂

非在研适应症-

最高研发阶段药物发现

首次获批国家/地区-

首次获批日期1800-01-20

100 项与 CBX1 相关的临床结果

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100 项与 CBX1 相关的转化医学

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0 项与 CBX1 相关的专利（医药）

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519

项与 CBX1 相关的文献（医药）

2024-10-01·Biochemical Genetics

Circ-NUP98 Promotes Lung Adenocarcinoma Development Through Regulating CBX1 by miR-188-3p

Article

作者: Liu, Guiju ; Mei, Jiazhuan ; Xiao, Peng ; Zuo, Jing ; Mei, Jie

Lung cancer has a high morbidity and mortality among malignant tumors, and lung adenocarcinoma (LUAD) is the main type of lung cancer. In recent years, circular RNAs (circRNAs) have been confirmed to play an important role in the generation and development of human cancer. However, the specific role and mechanism of circ-NUP98 in LUAD are still unclear and need to be further investigated. Circ-NUP98, microRNA-188-3p (miR-188-3p), and chromobox homolog 1 (CBX1) levels were detected by real-time quantitative polymerase chain reaction (RT-qPCR). Cell-counting Kit-8 (CCK-8), 5-Ethynyl-2'-deoxyuridine (EdU) assay, flow cytometry, wound healing, and transwell assay were used to observe LUAD cell proliferation, apoptosis, migration, invasion, and cell-cycle progression. Malondialdehyde (MDA) and superoxide dismutase (SOD) levels were examined using special assay kits. CyclinD1, Bcl-2-related X protein (Bax), matrix metalloproteinase 9 (MMP9) protein, and CBX1 protein levels were determined using Western blot. The interaction between miR-188-3p and circ-NUP98 or CBX1 was identified by dual-luciferase reporter and RNA immunoprecipitation (RIP) assay. In vivo efficacy of circ-NUP98 was evaluated in a xenograft tumor model. Besides, the expression of CBX1 and KI67 in the tumors was detected by immunohistochemical (IHC) assay. Circ-NUP98 and CBX1 expressions were upregulated in LUAD tissues and cells, and miR-188-3p was decreased. Downregulation of circ-NUP98 could inhibit the proliferation, migration, invasion, and oxidative stress, and promote apoptosis of LUAD cells. Mechanism experiments showed that circ-NUP98 acted as a sponge for miR-188-3p to increase CBX1 expression. Knockdown of circ-NUP98 could inhibit the growth of LUAD tumors in vivo. Circ-NUP98 might promote the malignant development of LUAD via the miR-188-3p/CBX1 axis, which might provide a potential new marker for early diagnosis of LUAD.

2024-09-01·Environmental Pollution

Neurotoxicity of tetrabromobisphenol-A-bis(2,3-dibromopropyl ether) through the GABAergic and serotonergic neurotransmission in Caenorhabditis elegans

Article

作者: Chen, Haibo ; Dang, Yao ; Guo, Hongzhi ; Yu, Yunjiang ; Xiang, Mingdeng ; Yang, Yue ; Xie, Dongli

Tetrabromobisphenol-A-bis(2,3-dibromopropyl ether) (TBBPA-BDBPE), a novel additive brominated flame retardant, is being developed for use in polyolefin and copolymers. Despite its emerging application, the neurotoxicity and mechanisms of action of TBBPA-BDBPE remain unexplored. Caenorhabditis elegans was utilized as the model organism to study the neurotoxic effects of TBBPA-BDBPE across environmental concentrations ranging from 0 to 100 μg/L. This investigation focused on various toxicological endpoints such as locomotive behavior, neuronal injury, neurotransmitter transmission, and the regulation of nervous system-related gene expression. Acute exposure to TBBPA-BDBPE at concentrations of 10-100 μg/L significantly impaired nematode movement, indicating potential neurotoxicity. In transgenic nematodes, this exposure also caused damage to γ-aminobutyric acid (GABAergic) and serotonergic neurons, along with notable changes in the levels of GABAergic and serotonergic neurotransmitters. Further molecular studies indicated alterations in neurotransmission-related genes (cat-4, mod-1, unc-25, and unc-47). Molecular docking analysis confirmed the binding affinity of TBBPA-BDBPE to key neurotransmission proteins-CAT-4, MOD-1, UNC-25, and UNC-47. These findings demonstrate that TBBPA-BDBPE exerts neurotoxic effects by impacting GABAergic and serotonergic neurotransmission in nematodes. This study provides new insights into the potential environmental risks of TBBPA-BDBPE.

2024-09-01·Psychiatria Danubina

Rapidly Trading Down Depression's 3 Pillars to 5HT3-Receptors Through ECT or Psilocybin?

Review

作者: Treviranus, Gottfried R S

Depression astonishingly can be stopped instantly by electrotherapies or through some psychedelics like psilocybin. In explaining this, the traditional approaches to their antidepressant effects via "reset" models and orthosteric serotonin receptors has neglected the only serotonin channel 5HT3, which e.g. has emerged as being helpful for the neurotrophic translation for all anti-depressants and final synaptic effects. Psychedelics here are confronted with a panorama of also anti-depressant 5HT3-channels and a search for their part e.g. in the "3 pillars" reigning depression. Of these M1) mitochondria, parasitic organelles from a fusion between some proto-bacteria and archae, founding eukaryotes, also through 5HT3 in depression determine much of its somatic crises. Two further pillars, "pushback" and "shame-link", are clarified by the parasympathetic (PS-) conspiciously 5HT3-rich "nasal" pterygo-palatine ganglion (PPG): PPG-1.) Intramural "pushbacks" intoxicating brain's tissues, show up on MRI e.g. along branches of the peri-/subcallosal artery. The brain-draining circular chambers, by CIMURAF, are plausibly driven by the PPG (and other PS-ganglia) through their dense nitrergic grid, causing loose wrung areas creating hyperboloid stenoses where they delimit contracted sliding segments PPG-2.) Existential conflicts trigger last-resort attacks, whereby the subduing are stopped into submissive shame. This plausibly occurs via the antidromic "Suzuki-link" from preparatory attack-biting (V3) via the trigeminal ggl. V3-V2-crosstalk onto the PPG, which, blushing via PACAP, maybe via MCs opens the BBB causing foggy confusion. Mushrooms may have acquired psilocybin to similarly stop feeding moves of worms (C. elegans) via the >100 5HT3-like ion channels. While on MOD-1 serotonin elicits "dwelling", collective feeding on just one fungus, psilocin could on promote audacious "roaming" (protecting fungi) - channel LGC-50 learning from this. The biphasic and pervasive H₂S, being a dipole, might be flushed by ECT and on the 5HT3-receptors might get worms (and us) to move.