EREG Target Analysis Report Summary
About the Target
Based on the context information provided, here are some key viewpoints related to ER (Endoplasmic Reticulum) and its various signaling pathways:
ER stress signaling pathways: The unfolded protein response (UPR) sensors, including IRE1, PERK, and ATF6, play crucial roles in responding to unfolded protein accumulation in the ER. Activation of these sensors leads to the induction of specific activities that regulate factors involved in apoptosis, mRNA decay, mRNA splicing, and global mRNA translation inhibition [1].
Golgi stress response: Besides the ER stress signaling pathways, there are also Golgi stress signaling pathways that have been discovered, although their characterization is currently limited [1].
Cotranslational protein import into the ER: The process of cotranslational mammalian protein import into the ER involves the Sec61 protein translocon, which allows the insertion of secreted proteins into the ER lumen or diffusion of integral membrane proteins into the ER lipid bilayer. Inhibitors such as Tunicamycin and cavinafungin can disrupt this process [2].
ER-endosome MCSs (Membrane Contact Sites): The sterol-transfer protein STARD3 plays a role in forming MCSs between late endosomes (LE) and the ER. These MCSs facilitate cholesterol transport and involve the interaction of STARD3 with integral ER proteins called VAPs. In cancer cells, overexpression of STARD3 can lead to the formation of aberrant MCSs and inhibit endosomal maturation [3].
ER stress and UPR in rosacea: Rosacea, a chronic inflammatory condition, can induce ER stress and activate the unfolded protein response in keratinocytes. This ER stress-mediated signaling can lead to the activation of innate immune responses, including the expression of TLR2 and KLK5, as well as excessive production of cathelicidin, which plays a role in the innate immune activation of rosacea [4].
FAM134B and Atlastin in ER content delivery to lysosomes: FAM134B and Atlastin are involved in macroER-phagy and ER-phagy-related ERLAD processes, which contribute to the clearance of specific ER lumenal moieties and the remodeling of the ER. These processes involve the recruitment of various proteins and interactions with autophagosomes and lysosomes [5].
It is worth noting that while the viewpoints provided are based on the given context information and can be useful for understanding ER-related processes, more comprehensive understanding might require further research and examination of additional sources.
Based on the given context information, here are some key viewpoints related to ER:
Calcium handling at the endoplasmic reticulum (ER) plays a crucial role in cellular processes such as virus replication and cell death pathways [6].
ER chaperones and proteins like IP3R, VDAC, sigma1R, and GRP78/BiP are involved in maintaining ER calcium homeostasis and regulating cell death processes [7].
ER forms contacts with various cellular organelles like lipid droplets (LDs), mitochondria, and peroxisomes, facilitating metabolite transfer and lipid synthesis [8].
The unfolded protein response (UPR) is an adaptive cellular mechanism that readjusts ER homeostasis, and persistent ER stress can lead to pro-apoptotic pathways [9].
There is crosstalk between the phosphatidylinositol-3-kinase (PI3K) pathway and estrogen receptor (ER), affecting ER-dependent transcription and activation of downstream effectors [10].
Note: The viewpoints provided are a summary of the information based on the given keywords and do not include any prior knowledge. References are provided in [number] notation after each viewpoint.
Figure [1]
Figure [2]
Figure [3]
Figure [4]
Figure [5]
Figure [6]
Figure [7]
Figure [8]
Figure [9]
Figure [10]
Note: If you are interested in the full version of this target analysis report, or if you'd like to learn how our AI-powered BDE-Chem can design therapeutic molecules to interact with the EREG target at a cost 90% lower than traditional approaches, please feel free to contact us at BD@silexon.ai.
More Common Targets
ABCB1 | ABCG2 | ACE2 | AHR | AKT1 | ALK | AR | ATM | BAX | BCL2 | BCL2L1 | BECN1 | BRAF | BRCA1 | CAMP | CASP3 | CASP9 | CCL5 | CCND1 | CD274 | CD4 | CD8A | CDH1 | CDKN1A | CDKN2A | CREB1 | CXCL8 | CXCR4 | DNMT1 | EGF | EGFR | EP300 | ERBB2 | EREG | ESR1 | EZH2 | FN1 | FOXO3 | HDAC9 | HGF | HMGB1 | HSP90AA1 | HSPA4 | HSPA5 | IDO1 | IFNA1 | IGF1 | IGF1R | IL17A | IL6 | INS | JUN | KRAS | MAPK1 | MAPK14 | MAPK3 | MAPK8 | MAPT | MCL1 | MDM2 | MET | MMP9 | MTOR | MYC | NFE2L2 | NLRP3 | NOTCH1 | PARP1 | PCNA | PDCD1 | PLK1 | PRKAA1 | PRKAA2 | PTEN | PTGS2 | PTK2 | RELA | SIRT1 | SLTM | SMAD4 | SOD1 | SQSTM1 | SRC | STAT1 | STAT3 | STAT5A | TAK1 | TERT | TLR4 | TNF | TP53 | TXN | VEGFA | YAP1
