HMGA Genes and Proteins in Development and Evolution

Vignali, Robert; Marracci, Silvia

doi:10.3390/ijms21020654

Cited by 61 publications

(51 citation statements)

References 295 publications

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“…ID2-which modulates bone morphogenetic protein (BMP) signalling during craniofacial development (Nimmagadda et al, 2015); LIN28Awhich may promote HMGA2 expression (Vignali & Marracci, 2020);…”

Section: Demographic Modelmentioning

confidence: 99%

An island‐hopping bird reveals how founder events shape genome‐wide divergence

et al. 2021

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The establishment of a new population involves phases of founding and recovery leading to long-term persistence. During each stage, the random sampling effect of drift has the potential to affect the degree of genetic diversity and divergence exhibited by a population . When populations are founded by few individuals, and especially when combined with longer population recovery times, there is the potential for loss of genetic variation-a "founder effect" (Nei et al., 1975;Wright, 1931). Loss of diversity has important implications on several fronts. For example, it may limit responses to new adaptive landscapes via loss of potentially adaptive

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Section: Demographic Modelmentioning

confidence: 99%

An island‐hopping bird reveals how founder events shape genome‐wide divergence

et al. 2021

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“…HMGA1 is a member of the HMG family of architectural transcription factors and involved in chromatin remodeling and regulation of different gene expression depending on the cell context. [ 30 ]. HMGA1 is abundantly expressed during embryo development and downregulated in the adult differentiated tissues.…”

Section: Discussionmentioning

confidence: 99%

LncRNA MALAT1 aggravates oxygen‐glucose deprivation/reoxygenation-induced neuronal endoplasmic reticulum stress and apoptosis via the miR-195a-5p/HMGA1 axis

Jia

et al. 2021

Biol Res

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Background This study aimed to investigate the potential role and molecular mechanism of lncRNA metastasis associated lung adenocarcinoma transcript 1 (MALAT1) in cerebral ischemia/reperfusion injury. Results Using an oxygen-glucose deprivation/reoxygenation (OGD/R) cell model, we determined that the expression of MALAT1 was significantly increased during OGD/R. MALAT1 knockdown reversed OGD/R-induced apoptosis and ER stress. Mechanistically, MALAT1 promoted OGD/R-induced neuronal injury through sponging miR-195a-5p to upregulating high mobility group AT-hook1 (HMGA1). Conclusions Collectively, these data demonstrate the mechanism underlying the invovlvement of MALAT1 in cerebral ischemia/reperfusion injury, thus providing translational evidence that MALAT1 may serve as a novel biomarker and therapeutic target for ischemic stroke.

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“…It contains three special at‐hook structures, which can bind to at‐sequence‐enriched regions on DNA, promote or inhibit the expression of related target genes, and thus affect the development of embryos 5 . Generally, HMGA2 is only highly expressed at the early stage of fetal development, and the expression of HMGA2 can hardly be detected in normal adult tissues 6,7 . A large number of studies have shown that HMGA2 is highly expressed in most malignant tumors, and its expression level is closely related to the degree of malignancy and metastasis, including breast, melanoma, colorectal and bladder cancer 8,9 .…”

Section: Introductionmentioning

confidence: 99%

P300‐dependent acetylation of histone H3 is required for epidermal growth factor receptor‐mediated high‐mobility group protein A2 transcription in hepatocellular carcinoma

et al. 2020

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High‐mobility group protein A2 (HMGA2) is highly expressed in hepatocellular carcinoma (HCC) cells and contributes to tumor metastasis and poor patient survival. However, the molecular mechanism through which HMGA2 is transcriptionally regulated in HCC cells remains largely unclear. Here, we showed that the expression HMGA2 was upregulated in HCC, and that elevated HMGA2 could promote tumor metastasis. Incubation of HCC cells with epidermal growth factor (EGF) could promote the expression of HMGA2 mRNA and protein. Mechanistic studies suggested that EGF can phosphorylate p300 at Ser1834 residue through the PI3K/Akt signaling pathway in HCC cells. Knockdown of p300 can reverse EGF‐induced HMGA2 expression and histone H3‐K9 acetylation, whereas a phosphorylation‐mimic p300 S1834D mutant can stimulate HMGA2 expression as well as H3‐K9 acetylation in HCC cells. Furthermore, we identified that p300‐mediated H3‐K9 acetylation participates in EGF‐induced HMGA2 expression in HCC. In addition, the levels of H3‐K9 acetylation positively correlated with the expression levels of HMGA2 in a chemically induced HCC model in rats and human HCC specimens.

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HMGA Genes and Proteins in Development and Evolution

Cited by 61 publications

References 295 publications

An island‐hopping bird reveals how founder events shape genome‐wide divergence

An island‐hopping bird reveals how founder events shape genome‐wide divergence

LncRNA MALAT1 aggravates oxygen‐glucose deprivation/reoxygenation-induced neuronal endoplasmic reticulum stress and apoptosis via the miR-195a-5p/HMGA1 axis

P300‐dependent acetylation of histone H3 is required for epidermal growth factor receptor‐mediated high‐mobility group protein A2 transcription in hepatocellular carcinoma

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