Last update 01 Nov 2024

Secretoglobin

Last update 01 Nov 2024

Basic Info

Synonyms-

Introduction-

Drugs associated with Secretoglobin

SCGB-3A2

Target

Secretoglobin

Mechanism

Secretoglobin stimulators

Active Org.

Therabron Therapeutics, Inc.

Originator Org.

Clarassance

Active Indication

Respiration Disorders

Inactive Indication

Bronchiectasis [+1]

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

HG-1298

Target

Secretoglobin

Mechanism

Selenoprotein modulators

Active Org.-

Originator Org.

Human Genome Sciences, Inc.

Active Indication-

Inactive Indication

Neoplasms

Drug Highest PhasePending

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with Secretoglobin

100 Translational Medicine associated with Secretoglobin

0 Patents (Medical) associated with Secretoglobin

Literatures (Medical) associated with Secretoglobin

01 Jul 2024·American Journal of Physiology-Lung Cellular and Molecular Physiology

NF-κB/RelA signaling in secretoglobin progenitors mediates plasticity and MMP-induced barrier disruption in house dust mite-induced allergic asthma

Article

Author: Brasier, Allan R. ; Skibba, Melissa E.

Allergic asthma from house dust mite (HDM) allergy causes substantial morbidity. This study examines the dynamic changes in small airway epithelial cells in a mouse model of HDM exposure. Our findings indicate that NF-κB/RelA signaling mediates matrix metalloproteinase production, disrupting the epithelial barrier resulting in allergic sensitization. Our findings bring new insight into mechanisms for epithelial cell-state change in the allergen response, creating a potential therapeutic pathway for maintaining barrier function in asthma.

01 Feb 2024·iScience

Circadian disruption during fetal development promotes pathological cardiac remodeling in male mice

Article

Author: Liu, Jing-Yu ; Tang, Ao-Xue ; Yang, Hui-Jiao ; Luo, Xiao-Qin ; Liu, Wei-Chao ; Yu, Yang ; Huang, Xiao-Xin ; Gao, Xiao-Ping ; Zhang, Peng ; Mary Cheng, Hai-Ying

Disruption of circadian rhythms during fetal development may predispose mice to developing heart disease later in life. Here, we report that male, but not female, mice that had experienced chronic circadian disturbance (CCD) in utero were more susceptible to pathological cardiac remodeling compared with mice that had developed under normal intrauterine conditions. CCD-treated males showed ventricular chamber dilatation, enhanced myocardial fibrosis, decreased contractility, higher rates of induced tachyarrhythmia, and elevated expression of biomarkers for heart failure and myocardial remodeling. In utero CCD exposure also triggered sex-dependent changes in cardiac gene expression, including upregulation of the secretoglobin gene, Scgb1a1, in males. Importantly, cardiac overexpression of Scgb1a1 was sufficient to induce myocardial hypertrophy in otherwise naive male mice. Our findings reveal that in utero CCD exposure predisposes male mice to pathological remodeling of the heart later in life, likely as a consequence of SCGB1A1 upregulation.

01 Feb 2024·General and Comparative Endocrinology

Estrogen regulated transcription of the non-estrogen-regulated hamster uteroglobin gene in MCF-7 cells

Article

Author: Enríquez, Juana ; Ulloa-Aguirre, Alfredo ; Cruz-Huerta, Edith ; Gutiérrez-Sagal, Rubén ; Zariñán, Teresa

To study the estrogen regulated transcription of the uteroglobin (UG) gene, the founding member of the secretoglobin family widely expressed in many different mammalian species, we re-created functional estrogen response elements (EREs) in the UG gene promoter from a species where UG expression is not regulated by estrogens: the hamster Mesocricetus auratus (Ma), to ascertain if the lack of functional EREs is the real cause of its estrogen insensitivity. Functional EREs in the hamster promoter, including the consensus ERE (cERE), failed to respond to an appropriate estrogen stimulus compared with its estrogen regulated ortholog from the brown hare Lepus capensis (Lc). As the nucleotide sequence is the only difference between genetic constructs from these two species, we suspected that the UG promoter from the hamster probably contains cis-acting genetic elements that negatively impairs the estrogen-regulated transcription mediated by the functional ERE. Accordingly, we prepared chimeric DNA constructs which eventually allowed to identify a region located 29 base pairs (bp) downstream of the ERE as responsible for the lack of estrogen-responsiveness of the Ma-UG gene in the breast cancer cell line MCF-7. This region contains the sequence ACACCCC which has been identified as the core sequence of the Sp/ Krüppel-like factor (KLF) family of transcription factors. This finding is relevant, not only due to the observation on a novel mechanism that control estrogen-induced transcription, but also because it may encourage further investigation for better defining specific genes with an ERE that do not respond to estrogen signaling in MCF-7 cells, a cell line widely employed as an in vitro model in breast cancer research.

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Secretoglobin

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