scholarly journals Cytokeratin 18 regulates the transcription and alternative splicing of apoptotic‑related genes and pathways in HeLa cells

2019 ◽  
Author(s):  
Yi Cheng ◽  
Kai Qin ◽  
Nan Huang ◽  
Zhipeng Zhou ◽  
Huihua Xiong ◽  
...  
Keyword(s):  
Alternative Splicing ◽  
Hela Cells ◽  
Cytokeratin 18

scholarly journals Silencing cytokeratin 18 gene inhibits intracellular replication of Trypanosoma cruzi in HeLa cells but not binding and invasion of trypanosomes

2008 ◽  
Vol 9 (1) ◽  
Author(s):  
Carla Claser ◽  
Marli Curcio ◽  
Samanta M de Mello ◽  
Eduardo V Silveira ◽  
Hugo P Monteiro ◽  
...  
Keyword(s):  
Trypanosoma Cruzi ◽  
Hela Cells ◽  
Intracellular Replication ◽  
Cytokeratin 18

Exip, a New Alternative Splicing Variant of p38α, Can Induce an Earlier Onset of Apoptosis in HeLa Cells

2002 ◽  
Vol 291 (4) ◽  
pp. 838-843 ◽  
Author(s):  
Tatsuhiko Sudo ◽  
Yuki Yagasaki ◽  
Hiroshi Hama ◽  
Naoko Watanabe ◽  
Hiroyuki Osada
Keyword(s):  
Alternative Splicing ◽  
Hela Cells ◽  
Splicing Variant ◽  
Alternative Splicing Variant

Alternative splicing of the mouse profilin II gene generates functionally different profilin isoforms

2000 ◽  
Vol 113 (21) ◽  
pp. 3795-3803 ◽  
Author(s):  
A. Di Nardo ◽  
R. Gareus ◽  
D. Kwiatkowski ◽  
W. Witke
Keyword(s):  
Alternative Splicing ◽  
Cell Motility ◽  
Hela Cells ◽  
The Other ◽  
Actin Dynamics ◽  
High Affinity ◽  
Other Hand ◽  
The Brain

Profilins are a conserved family of proteins participating in actin dynamics and cell motility. In the mouse, two profilin genes are known. Profilin I is expressed universally at high levels, while profilin II is expressed mainly in the brain. Here we describe the occurrence of two mouse profilin II isoforms, A and B, which are derived by alternative splicing. They are identical through residue 107 of the protein, but then have distinct C-terminal sequences. Profilin IIA binds to poly-L-proline and actin with high affinity similar to profilin I. Profilin IIB on the other hand does not bind to actin and the affinity for poly-L-proline is greatly diminished. However, tubulin was found to bind to GST-profilin IIB, and in vivo GFP-profilin IIB was recruited to spindles and asters during mitosis in HeLa cells. Our results indicate unexpected diversity in the functions of the profilin family of proteins, and suggest that in mouse profilin IIA is intimately involved in actin dynamics, while profilin IIB associates with other cytoskeletal components.

scholarly journals Filamin B extensively regulates transcription and alternative splicing, and is associated with apoptosis in HeLa cells

2020 ◽  
Author(s):  
Hai‑Rong Ma ◽  
Li Cao ◽  
Fei Wang ◽  
Chao Cheng ◽  
Rendong Jiang ◽  
...  
Keyword(s):  
Alternative Splicing ◽  
Hela Cells ◽  
Filamin B

Functional Analysis of SRSF2 Mutations in Myelodysplastic Syndromes and Related Disorders

Blood ◽  
2011 ◽  
Vol 118 (21) ◽  
pp. 1706-1706
Author(s):  
Ayana Kon ◽  
Masashi Sanada ◽  
Kenichi Yoshida ◽  
Yasunobu Nagata ◽  
Yuichi Shiraishi ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Cell Proliferation ◽  
Alternative Splicing ◽  
Hela Cells ◽  
Rna Splicing ◽  
Sr Proteins ◽  
Wild Type ◽  
Functional Studies ◽  
Rs Domains

Abstract Abstract 1706 The recent study of whole-exome sequencing on MDS has revealed frequent and specific pathway mutations involving multiple components of the RNA splicing machinery, including U2AF35, SRSF2, SF3B1 and ZRSR2. The mutually exclusive manner of these mutations among MDS cases also supported that deregulated RNA splicing contributes to the pathogenesis of MDS. Interestingly, the distribution of these splicing pathway mutations shows a substantial difference with regard to disease subtypes. Thus, the SF3B1 mutations are by far the most frequent in RARS and RCMD-RS cases, and the SRSF2 mutations are more prevalent in CMML. SRSF2 is a member of the SR protein family that is commonly characterized by one or two RNA recognition motifs (RRM) and a signature serine/arginine-rich domains (RS domains). The SR proteins interact with other spliceosome components through their RS domains, among which most extensively characterized are SRSF1 (ASF/SF2) and SRSF2 (SC35). Both SR proteins bind a splicing enhancer site within the 3' target exon and also interact with the U2AF, playing an indispensable role in both constitutive and alternative splicing in most cell types. In fact, the knockout of these genes in mice results in embryonic lethality. There is emerging evidence that establishes a connection between the abnormal expression of SR proteins and the development of cancer, mainly as a result of change in the alternative splicing patterns of key transcripts. Increased expression of SR proteins usually correlates with cancer progression, as shown by elevated expression of SR proteins in ovarian cancer and breast cancer. In spite of the similarity in their functions, both proteins are thought to have distinct roles, especially in the pathogenesis of myeloid malignancies, since we found no SRSF1 mutations among 582 cases with myeloid neoplasms. On the other hand, studies have shown that increased expression of SRSF1 transforms immortal rodent fibroblasts and leads to the formation of sarcomas in nude mice, supporting the notion that SRSF1 is a proto-oncogene, whereas SRSF2 does not have transforming activity, indicating a highly specific role of SRSF1 in this type of cancer. Thus, little is known about the biological mechanism by which the SRSF2 mutations are involved in the pathogenesis of MDS, although the mutations at the P95 site are predicted to cause a significant displacement of the RS domain relative to the domain for RNA binding. So to gain an insight into the functional aspect of SRSF2 mutations, we performed sequencing analysis of mRNAs extracted from mutant (P95H) SRSF2-transduced HeLa cells in which expression of the wild-type and mutant SRSF2 were induced by doxycycline. The abnormal splicing in mutant SRSF2-transduced cells was directly demonstrated by evaluating the read counts in different fractions. Next, to investigate functional role of SRSF2 mutant, HeLa cells were transduced with lentivirus constructs expressing either the P95H SRSF2 mutant or wild-type SRSF2, and cell proliferation was examined. After the induction of gene expression, the mutant SRSF2-transduced cells showed reduced cell proliferation. In addition, we transduced P95H SRSF2 constructs into factor-dependent 32D cell lines. The expression of mutant SRSF2 protein resulted in increased apoptosis in the presence of IL-3 and also suppression of cell growth in the presence of G-CSF, which may be related to ineffective hematopoiesis, a common feature of MDS. To further clarify the biological effect of SRSF2 mutants in vivo, a highly purified hematopoietic stem cell population (CD34-c-Kit+ScaI+ Lin-) prepared from C57BL/6 (B6)-Ly5.1 mouse bone marrow was retrovirally transduced with either the mutant or wild-type SRSF2 with EGFP marking. The transduced cells were mixed with whole bone marrow cells from B6-Ly5.1/5.2 F1 mice, transplanted into lethally irradiated B6-Ly5.2 recipients, and we are now monitoring the ability of these transduced cells to reconstitute the hematopoietic system and other hematological phenotypes. Much remains, however, to be unrevealed about the functional link between the abnormal splicing of RNA species and the phenotype of myelodysplasia. Further functional studies should be warranted to understand these mechanisms in detail. In this meeting, we will present the results of our functional studies on the SRSF2 mutations and discuss the pathogenesis of MDS in terms of the alterations of splicing machinery. Disclosures: No relevant conflicts of interest to declare.

RBM4 modulates the proliferation and expression of inflammatory factors via the alternative splicing of regulatory factors in HeLa cells

2019 ◽  
Vol 295 (1) ◽  
pp. 95-106 ◽  
Author(s):  
Wei-Yang Wang ◽  
Weili Quan ◽  
Fan Yang ◽  
Ya-Xun Wei ◽  
Jia-Jun Chen ◽  
...  
Keyword(s):  
Alternative Splicing ◽  
Hela Cells ◽  
Inflammatory Factors ◽  
Regulatory Factors

scholarly journals ATP5A1 Participates in Transcriptional and Posttranscriptional Regulation of Cancer-Associated Genes by Modulating Their Expression and Alternative Splicing Profiles in HeLa Cells

2021 ◽  
Vol 20 ◽  
pp. 153303382110391
Author(s):  
Yisa Song, BA ◽  
Fei Wang, MA ◽  
Yaxun Wei, MA ◽  
Dong Chen, BA ◽  
Gang Deng, BA
Keyword(s):  
Gene Expression ◽  
Alternative Splicing ◽  
Cancer Cells ◽  
Cancer Progression ◽  
Hela Cells ◽  
Posttranscriptional Regulation ◽  
Aberrant Expression ◽  
Qpcr Analysis ◽  
Mitochondrial Atp Synthase ◽  
Signaling Activation

Background: Aberrant expression and alternative splicing of oncogenes are the driving events in tumor initiation and development. But how these events are regulated in cancer cells is largely unknown. Functions of ATP5A1, an important mitochondrial ATP synthase gene, in transcriptional and posttranscriptional regulation were explored in this study. Methods: ATP5A1 was overexpressed using plasmid-transformed HeLa cells, and its influence on cell apoptosis and proliferation is evaluated. Transcriptome sequencing was then performed using RNA-seq to study the changes in gene expression and regulation of alternative splicing events. Validation of the implicated genes was achieved using RT-qPCR analysis. Results: It was found that ATP5A1 could significantly promote cellular apoptosis, but it had no influence on cell proliferation. ATP5A1 overexpression significantly increased the expression levels of genes associated with the innate immune response, angiogenesis, and collagen catabolic processes. This included enrichment of MMP2 and MMP19. It was also found that ATP5A1 could interfere with the alternative splicing of hundreds of genes associated with glucose homeostasis, HIF-1 signaling activation, and several pathways associated with cancers. Eight ATP5A1-regulated differentially expressed genes and 3 genes altered by splicing were selected and validated using RT-qPCR analysis. Conclusions: In summary, we illustrate the regulatory functions of ATP5A1 on the transcriptome of HeLa cells by exploring its influence on gene expression and alternative splicing. The results suggest that ATP5A1 may play an important regulatory role in cervical cancer cells by regulating expression and alternative splicing of cancer-associated genes. This study provides novel insights into the current understanding of the mechanisms of ATP5A1 on carcinogenesis and cancer progression.

CELF1 preferentially binds to exon-intron boundary and regulates alternative splicing in HeLa cells

2017 ◽  
Vol 1860 (9) ◽  
pp. 911-921 ◽  
Author(s):  
Heng Xia ◽  
Dong Chen ◽  
Qijia Wu ◽  
Gang Wu ◽  
Yanhong Zhou ◽  
...  
Keyword(s):  
Alternative Splicing ◽  
Hela Cells ◽  
Intron Boundary

scholarly journals Expression proteomics of UPF1 knockdown in HeLa cells reveals autoregulation of hnRNP A2/B1 mediated by alternative splicing resulting in nonsense-mediated mRNA decay

BMC Genomics ◽  
2010 ◽  
Vol 11 (1) ◽  
Author(s):  
Nicholas J McGlincy ◽  
Lit-Yeen Tan ◽  
Nicodeme Paul ◽  
Mihaela Zavolan ◽  
Kathryn S Lilley ◽  
...  
Keyword(s):  
Alternative Splicing ◽  
Hela Cells ◽  
Mrna Decay ◽  
Nonsense Mediated Mrna Decay
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