Temporally and Spatially Regulated Expression of the Linker Histone H1fx During Mouse Development

Ichihara-Tanaka, Keiko; Kadomatsu, Kenji; Kishida, Satoshi

doi:10.1369/0022155417723914

Cited by 6 publications

(4 citation statements)

References 42 publications

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“…NCL preferentially binds to H3K4Me2 and not H3K4Me3 23. H1FX is usually associated with the poorly acetylated core histone-enriched regions of genomic DNA 12, 24, 25, but has low binding affinity for promoters with highly acetylated histones 26. We showed that AY significantly enriched H3K4me3 and acH3K9K14 on the ITGAV promoter.…”

Section: Discussionmentioning

confidence: 69%

LncRNA AY promotes hepatocellular carcinoma metastasis by stimulating ITGAV transcription

Kang

Cai

et al. 2019

Theranostics

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Rationale : Tumor metastasis is the main cause for cancer-related death. However, the driving molecules of metastasis remain largely unknown. Here, we aim to identify long non-coding RNAs (lncRNAs) critical for human hepatocellular carcinoma (HCC) metastasis. Methods : Microarrays were used to screen a comprehensive set of lncRNAs with differential expression profiles in sulfatide-treated cells. Mass spectrometry, protein arrays, and RNA pull-down experiments were used to identify proteins that interacted with lncRNA. Epigenetic analysis was used to study lncRNA-mediated regulation mechanisms. Results : We identified lncRNA AY927503 (AY) as a metastasis-associated molecule that was highly expressed in human hepatocellular carcinoma (HCC) and correlated with metastatic events and poor prognosis in patients with HCC. AY promoted HCC cell migration, stemness, 5-fluorouracil resistance, and metastasis in mice. However, knockdown of integrin αV (ITGAV) abolished AY-stimulated migration, cell viability in HCC cells or tube formation. AY strongly promoted ITGAV transcription and αVβ3 expression by interacting with the ITGAV promoter specifically and stimulating its activity. AY was identified to interact with histone 1FX (H1FX), but deletion of the central domain of AY (AY∆371-522) abolished H1FX binding and ITGAV promoter stimulation. AY significantly enriched H3K4Me3 and acH3K9/14 but reduced H3K27Me3 and H1FX occupancy on the ITGAV promoter, which remodeled chromatin structures for RNA polymerase II recruitment. Knockdown of H1FX abrogated ITGAV transcription stimulated by AY. Conclusions : Our findings suggested that lncRNA AY promoted HCC metastasis via induction of chromatin modification for ITGAV transcription as a pioneer factor and was a potential molecular signature for metastasis or poor prognosis in patients with HCC.

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Section: Discussionmentioning

confidence: 69%

LncRNA AY promotes hepatocellular carcinoma metastasis by stimulating ITGAV transcription

Kang

Cai

et al. 2019

Theranostics

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“…Furthermore, Zhang and colleagues suggest that continuous light causes post-translational modification of Vim and indolamine melatonin reverts the vimentin modification to the original form 44 . Histone H1.0 (H1f0) is a member of the H1 histone family of nuclear proteins which are a component of chromatin in eukaryotic cells 45 . Splicing factor, proline- and glutamine-rich (Sfpq) controls cell growth and regulates apoptosis-related genes 46 .…”

Section: Discussionmentioning

confidence: 99%

Interaction of melatonin and Bmal1 in the regulation of PI3K/AKT pathway components and cellular survival

Beker

Çağlayan

Keleştemur

et al. 2019

Sci Rep

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The circadian rhythm is driven by a master clock within the suprachiasmatic nucleus which regulates the rhythmic secretion of melatonin. Bmal1 coordinates the rhythmic expression of transcriptome and regulates biological activities, involved in cell metabolism and aging. However, the role of Bmal1 in cellular- survival, signaling, its interaction with intracellular proteins, and how melatonin regulates its expression is largely unclear. Here we observed that melatonin increases the expression of Bmal1 and both melatonin and Bmal1 increase cellular survival after oxygen glucose deprivation (OGD) while the inhibition of Bmal1 resulted in the decreased cellular survival without affecting neuroprotective effects of melatonin. By using a planar surface immunoassay for PI3K/AKT signaling pathway components, we revealed that both melatonin and Bmal1 increased phosphorylation of AKT, ERK-1/2, PDK1, mTOR, PTEN, GSK-3αβ, and p70S6K. In contrast, inhibition of Bmal1 resulted in decreased phosphorylation of these proteins, which the effect of melatonin on these signaling molecules was not affected by the absence of Bmal1. Besides, the inhibition of PI3K/AKT decreased Bmal1 expression and the effect of melatonin on Bmal1 after both OGD in vitro and focal cerebral ischemia in vivo. Our data demonstrate that melatonin controls the expression of Bmal1 via PI3K/AKT signaling, and Bmal1 plays critical roles in cellular survival via activation of survival kinases.

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“…DOCK8 deficiencies impair immune cell migration in both the innate and adaptive immune system ( 21 ). Changes in psoriatic Trm also include elevated transcripts levels of the linker histone H1FX ( 22 ), histone chaperone NAP1L4 ( 23 ), and the chromatin-modifying enzyme SMARCA5 ( 24 ). Figure 4B globally displays psoriasis Trm2 abnormalities in these four programs on a per-patient level.…”

Section: Resultsmentioning

confidence: 99%

Defining Patient-Level Molecular Heterogeneity in Psoriasis Vulgaris Based on Single-Cell Transcriptomics

et al. 2022

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Identifying genetic variation underlying human diseases establishes targets for therapeutic development and helps tailor treatments to individual patients. Large-scale transcriptomic profiling has extended the study of such molecular heterogeneity between patients to somatic tissues. However, the lower resolution of bulk RNA profiling, especially in a complex, composite tissue such as the skin, has limited its success. Here we demonstrate approaches to interrogate patient-level molecular variance in a chronic skin inflammatory disease, psoriasis vulgaris, leveraging single-cell RNA-sequencing of CD45+ cells isolated from active lesions. Highly psoriasis-specific transcriptional abnormalities display greater than average inter-individual variance, nominating them as potential sources of clinical heterogeneity. We find that one of these chemokines, CXCL13, demonstrates significant correlation with severity of lesions within our patient series. Our analyses also establish that genes elevated in psoriatic skin-resident memory T cells are enriched for programs orchestrating chromatin and CDC42-dependent cytoskeleton remodeling, specific components of which are distinctly correlated with and against Th17 identity on a single-cell level. Collectively, these analyses describe systematic means to dissect cell type- and patient-level differences in cutaneous psoriasis using high-resolution transcriptional profiles of human inflammatory disease.

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Temporally and Spatially Regulated Expression of the Linker Histone H1fx During Mouse Development

Cited by 6 publications

References 42 publications

LncRNA AY promotes hepatocellular carcinoma metastasis by stimulating ITGAV transcription

LncRNA AY promotes hepatocellular carcinoma metastasis by stimulating ITGAV transcription

Interaction of melatonin and Bmal1 in the regulation of PI3K/AKT pathway components and cellular survival

Defining Patient-Level Molecular Heterogeneity in Psoriasis Vulgaris Based on Single-Cell Transcriptomics

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