GRAMD2A

Last update 08 May 2025

Basic Info

Synonyms

GRAM domain containing 2A, GRAM domain-containing protein 2A, GRAMD2

+ [1]

Introduction

Participates in the organization of endoplasmic reticulum-plasma membrane contact sites (EPCS) with pleiotropic functions including STIM1 recruitment and calcium homeostasis. Constitutive tether that co-localize with ESYT2/3 tethers at endoplasmic reticulum-plasma membrane contact sites in a phosphatidylinositol lipid-dependent manner. Pre-marks the subset of phosphtidylinositol 4,5-biphosphate (PI(4,5)P2)-enriched EPCS destined for the store operated calcium entry pathway (SOCE).

100 Clinical Results associated with GRAMD2A

100 Translational Medicine associated with GRAMD2A

0 Patents (Medical) associated with GRAMD2A

Literatures (Medical) associated with GRAMD2A

01 Dec 2023·Cell Reports

Alveolar type I cells can give rise to KRAS-induced lung adenocarcinoma

Article

Author: Zhou, Beiyun ; Shen, Hua ; Borok, Zea ; Yang, Minxiao ; Ryan, Amy L ; Marconett, Crystal N ; Neely, Aaron ; Liu, Yixin ; Bassiouni, Rania ; Stueve, Theresa Ryan ; Carpten, John ; Wallace, W Dean ; Mullen, Daniel J ; Flodby, Per ; Castaldi, Alessandra ; Koss, Michael D ; Castillo, Jonathan ; Jashashvili, Tea ; Ogbolu, Ezuka

Lung adenocarcinoma (LUAD) is the most prevalent subtype of lung cancer and presents clinically with a high degree of biological heterogeneity and distinct clinical outcomes. The current paradigm of LUAD etiology posits alveolar epithelial type II (AT2) cells as the primary cell of origin, while the role of AT1 cells in LUAD oncogenesis remains unknown. Here, we examine oncogenic transformation in mouse Gram-domain containing 2 (Gramd2)⁺ AT1 cells via oncogenic KRAS^G12D. Activation of KRAS^G12D in AT1 cells induces multifocal LUAD, primarily of papillary histology. Furthermore, KRT8⁺ intermediate cell states were observed in both AT2- and AT1-derived LUAD, but SCGB3A2⁺, another intermediate cell marker, was primarily associated with AT1 cells, suggesting different mechanisms of tumor evolution. Collectively, our study reveals that Gramd2⁺ AT1 cells can serve as a cell of origin for LUAD and suggests that distinct subtypes of LUAD based on cell of origin be considered in the development of therapeutics.

01 Oct 2020·American Journal of Physiology-Lung Cellular and Molecular PhysiologyQ2 · MEDICINE

Prenatal smoke exposure dysregulates lung epithelial cell differentiation in mouse offspring: role for AREG-induced EGFR signaling

Q2 · MEDICINE

Article

Author: Song, Shanshan ; Lkhagvadorj, Khosbayar ; Kooistra, Wierd ; Krauss-Etschmann, Susanne ; Cao, Junjun ; Hylkema, Machteld N. ; Zeng, Zhijun ; Melgert, Barbro N. ; Reinders-Luinge, Marjan ; Song, Juan

Prenatal smoke exposure is a risk factor for impaired lung development in children. Recent studies have indicated that amphiregulin (AREG), which is a ligand of the epidermal growth factor receptor (EGFR), has a regulatory role in airway epithelial cell differentiation. In this study, we investigated the effect of prenatal smoke exposure on lung epithelial cell differentiation and linked this with AREG-EGFR signaling in 1-day-old mouse offspring. Bronchial and alveolar epithelial cell differentiations were assessed by immunohistochemistry. Areg, epidermal growth factor ( Egf), and mRNA expressions of specific markers for bronchial and alveolar epithelial cells were assessed by RT-qPCR. The results in neonatal lungs were validated in an AREG-treated three-dimensional mouse lung organoid model. We found that prenatal smoke exposure reduced the number of ciliated cells and the expression of the cilia-related transcription factor Foxj1, whereas it resulted in higher expression of mucus-related transcription factors Spdef and Foxm1 in the lung. Moreover, prenatally smoke-exposed offspring had higher numbers of alveolar epithelial type II cells (AECII) and lower expression of the AECI-related Pdpn and Gramd2 markers. This was accompanied by higher expression of Areg and lower expression of Egf in prenatally smoke-exposed offspring. In bronchial organoids, AREG treatment resulted in fewer ciliated cells and more basal cells when compared with non-treated bronchiolar organoids. In alveolar organoids, AREG treatment led to more AECII cells than non-treated AECII cells. Taken together, the observed impaired bronchial and alveolar cell development in prenatally smoke-exposed neonatal offspring may be induced by increased AREG-EGFR signaling.

01 Mar 2020·The American Journal of Clinical NutritionQ1 · MEDICINE

Maternal fatty acid concentrations and newborn DNA methylation

Q1 · MEDICINE

Article

Author: Radoc, Jeannie G ; Mumford, Sunni L ; Flannagan, Kerry ; Trinh, Mai-Han ; Kim, Keewan ; Yeung, Edwina ; Zeng, Xuehuo ; Schisterman, Enrique F ; Robinson, Sonia L ; Guan, Weihua

BACKGROUNDPreconception nutrition sets the stage for a healthy pregnancy. Maternal fatty acids (FAs) are related to beneficial neonatal outcomes with DNA methylation proposed as a mechanism; however, few studies have investigated this association and none with preconception FAs.OBJECTIVESWe examined the relations of maternal plasma FA concentrations at preconception (n = 346) and 8 weeks of gestation (n = 374) with newborn DNA methylation.METHODSThe Effects of Aspirin in Gestation and Reproduction Trial (2006-2012) randomly assigned women with previous pregnancy loss to low dose aspirin or placebo prior to conception. We measured maternal plasma phospholipid FA concentration at preconception (on average 4 mo before pregnancy) and 8 weeks of gestation. Cord blood DNA from singletons was measured using the MethylationEPIC BeadChip. We used robust linear regression to test the associations of FA concentration with methylation β-values of each CpG site, adjusting for estimated cell count using a cord blood reference, sample plate, maternal sociodemographic characteristics, cholesterol, infant sex, and epigenetic-derived ancestry. False discovery rate correction was used for multiple testing.RESULTSMean ± SD concentrations of preconception marine (20:5n-3+22:6n-3+22:5n-3) and ω-6 PUFAs, SFAs, MUFAs, and trans FAs were 4.7 ± 1.2, 38.0 ± 2.0, 39.4 ± 1.8, 11.6 ± 1.1, and 1.0 ± 0.4 % of total FA, respectively; concentrations at 8 weeks of gestation were similar. Preconception marine PUFA concentration was associated with higher methylation at GRAMD2 (P = 1.1 × 10-8), LOXL1 (P = 5.5 × 10-8), SIK3 (P = 1.6 × 10-7), HTR1B (P = 1.9 × 10-7), and MCC (P = 2.1 × 10-7) genes. Preconception SFA concentration was associated with higher methylation at KIF25-AS1 and lower methylation at SLC39A14; other associations exhibited sensitivity to outliers. The trans FA concentration was related to lower methylation at 3 sites and higher methylation at 1 site. FAs at 8 weeks of gestation were largely unrelated to DNA methylation.CONCLUSIONSMaternal preconception FAs are related to newborn DNA methylation of specific CpG sites, highlighting the importance of examining nutritional exposures preconceptionally. This trial was registered at clinicaltrials.gov as NCT00467363.

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GRAMD2A

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