xfect transfection (TaKaRa)
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TaKaRa
xfect transfection
Xfect Transfection, supplied by TaKaRa, used in various techniques. Bioz Stars score: 96/100, based on 1306 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/xfect+reagent/Xfect+Transfection+Reagent/pmc13103552-42-0-4
Average 96 stars, based on 1306 article reviews
Xfect Transfection, supplied by TaKaRa, used in various techniques. Bioz Stars score: 96/100, based on 1306 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/xfect+reagent/Xfect+Transfection+Reagent/pmc13103552-42-0-4
Average 96 stars, based on 1306 article reviews
xfect transfection - by Bioz Stars,
2026-09
96/100 stars
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Transfection:Article Title: Overexpression of βTrCP1 elicits cell death in cisplatin-induced senescent cells. Article Snippet: .. MATERIALS AND METHODS Plasmids and viral transductions pLenti 6.3 HA βTrCP1, previously described [51], along with pMD2-G, pMDLg-pRRE and pRSV-Rev from Addgene (Watertown, MA, USA), were transfected into HEK293T cells using Article Title: Targeting Melanin Heterogeneity in Metastatic Melanoma: A Dual‐Tumour Mouse Melanoma Model Article Snippet: Cell culture reagents were purchased from Gibco, Fisher scientific, France, Strasbourg. .. B16‐OVA cells were transfected using Article Title: Chemical Targeting of the ATXN1 aa99–163 Interaction Site Suppresses polyQ-Expanded Protein Dimerization Article Snippet: .. Transfection was performed using Article Title: Overexpression of βTrCP1 elicits cell death in cisplatin-induced senescent cells Article Snippet: .. pLenti 6.3 HA βTrCP1, previously described [ ], along with pMD2-G, pMDLg-pRRE and pRSV-Rev from Addgene (Watertown, MA, USA), were transfected into HEK293T cells using Article Title: Palmitic acid fuels triple-negative breast cancer through metadherin-dependent fatty acid β-oxidation: Relevance to high fat diet-induced breast cancer progression. Article Snippet: Diets rich in saturated fats, specifically palmitic acid (PA), are associated with increased breast cancer risk.. However, the exact mechanisms linking dietary fat and cancer progression remain unclear.. Herein, we show that PA increases the levels of metadherin (MTDH), an oncogene, and its spliced isoform MTDHΔ7 in triple-negative breast cancer (TNBC) cells. Article Title: Regulatory grammar in human promoters uncovered by MPRA-based deep learning. Article Snippet: .. HAP1 was transfected using Article Title: Targeting Melanin Heterogeneity in Metastatic Melanoma: A Dual-Tumour Mouse Melanoma Model. Article Snippet: Cell culture reagents were purchased from Gibco, Fisher scientific, France, Strasbourg. .. B16- OVA cells were transfected using Article Title: Ubiquitylome Rewiring by Bacterial E3 Ligases Reveals Multifaceted Host Subversion Article Snippet: .. For transient transfection assays, Plasmid Preparation:Article Title: Targeting Melanin Heterogeneity in Metastatic Melanoma: A Dual‐Tumour Mouse Melanoma Model Article Snippet: Cell culture reagents were purchased from Gibco, Fisher scientific, France, Strasbourg. .. B16‐OVA cells were transfected using Article Title: Targeting Melanin Heterogeneity in Metastatic Melanoma: A Dual-Tumour Mouse Melanoma Model. Article Snippet: Cell culture reagents were purchased from Gibco, Fisher scientific, France, Strasbourg. .. B16- OVA cells were transfected using CRISPR:Article Title: Targeting Melanin Heterogeneity in Metastatic Melanoma: A Dual‐Tumour Mouse Melanoma Model Article Snippet: Cell culture reagents were purchased from Gibco, Fisher scientific, France, Strasbourg. .. B16‐OVA cells were transfected using Article Title: Targeting Melanin Heterogeneity in Metastatic Melanoma: A Dual-Tumour Mouse Melanoma Model. Article Snippet: Cell culture reagents were purchased from Gibco, Fisher scientific, France, Strasbourg. .. B16- OVA cells were transfected using Multiple Displacement Amplification:Article Title: Palmitic acid fuels triple-negative breast cancer through metadherin-dependent fatty acid β-oxidation: Relevance to high fat diet-induced breast cancer progression. Article Snippet: Diets rich in saturated fats, specifically palmitic acid (PA), are associated with increased breast cancer risk.. However, the exact mechanisms linking dietary fat and cancer progression remain unclear.. Herein, we show that PA increases the levels of metadherin (MTDH), an oncogene, and its spliced isoform MTDHΔ7 in triple-negative breast cancer (TNBC) cells. |
![(A) Heat map of differentially expressed genes identified by RNA-seq analysis comparing LINC00941 knockdown and control cells. Heat map showing expression of the same set of differentially expressed genes obtained from microarray analysis comparing siLINC00941 and siNT conditions using two independent siRNAs. (B) Volcano plot showing differentially expressed genes following LINC00941 knockdown in H1299 cells. Cells were transfected with two independent siRNAs targeting LINC00941 or four non-targeting siRNAs (siNT) for 48 h prior to RNA isolation and RNA sequencing. (c) KEGG pathway enrichment analysis of differentially expressed genes upon LINC00941 knock-down. Bar height indicates enrichment score and colour represents − log 10 ( P value). (D) Pre-ranked gene set enrichment analysis (GSEA) using Hallmark gene sets based on RNA-seq data. DNA replication and double-strand break repair pathways were among the most significantly negatively enriched gene sets following LINC00941 depletion. (E) Comet assay performed in control and LINC00941-depleted H1299 cells 48 h post-transfection. Representative images are shown and tail length was quantified using Comet Analyser software. (F) Immunoblot analysis of DNA damage response signalling proteins in H1299 cells treated with siNT, siLINC00941, ASO-NT, or ASO-LINC00941, demonstrating reduced activation of DDR pathways upon LINC00941 knockdown. (G) Immunofluorescence staining of γ H2AX in control and siLINC00941-treated H1299 cells. Representative images are shown and γ H2AX foci were quantified, revealing a significant reduction in foci number following LINC00941 depletion. (H) RNA fluorescence in situ hybridisation (RNA-FISH) analysis of LINC00941 localisation in H1299 cells. Probes targeting LINC00941 exons were labelled with Cy3 (green), and intronic probes were labelled with Cy5 (red). Nuclei were counterstained with DAPI. LINC00941 signal was detected in both the nuclear and cytoplasmic compartments as evident from the merged image. (I) Subcellular fractionation of H1299 cells followed by quantitative RT-PCR analysis of LINC00941 expression in nuclear and cytoplasmic fractions. H19 and HOTAIR were used as control lncRNAs for cytoplasmic and nuclear localisation, respectively. (J) RNA stability assay in H1299 cells treated with the transcriptional inhibitor actinomycin D. RNA was isolated at the indicated time points and LINC00941 expression was measured by quantitative RT-PCR and normalised to actin mRNA. (K) Schematic overview of the experimental workflow used to identify LINC00941-interacting proteins in whole-cell, nuclear, and cytoplasmic fractions. In vitro -transcribed, biotin-labelled LINC00941 RNA was incubated with cell lysates, followed by streptavidin pulldown and mass spectrometry analysis. (L) Table listing proteins enriched in LINC00941 pulldown samples from whole-cell, nuclear, and cytoplasmic lysates as identified by mass spectrometry. (M) Venn diagram showing overlap of LINC00941-associated proteins across nuclear and cyto-plasmic fractions. KHDRBS1 (SAM68) was uniquely enriched in the nuclear fraction, whereas QKI was enriched in the cytoplasmic fraction. (N) Bar graph depicting spectral counts from RNA immunoprecipitation (RIP), showing FAM120A binding to LINC00941 and [Control RNA] across nuclear, cytoplasmic, and whole-cell fractions. FAM120A demonstrated robust association with LINC00941 in all three fractions, while binding to [Control RNA] was negligible, confirming the specificity of the FAM120A–LINC00941 interaction. (O) Violin plot illustrating the differential expression of FAM120A protein in patient samples stratified by LINC00941 expression levels (high versus low). FAM120A expression was significantly elevated in LINC00941-high samples compared to LINC00941-low samples, indicating a positive correlation between FAM120A abundance and LINC00941 expression in clinical specimens. (P) Bar graph showing LINC00941 RNA and FAM120A RNA levels upon FAM120A knockdown relative to control cells. FAM120A depletion resulted in a significant reduction in LINC00941 RNA abundance, suggesting that FAM120A positively regulates LINC00941 expression or stability. (Q) RT-qPCR analysis of LINC00941 RNA expression in nuclear and cytoplasmic fractions of H1299 cells following FAM120A knockdown. RNA levels are presented relative to control. (R) Actinomycin D chase assay in control and FAM120A-depleted H1299 cells. Transcription was blocked with actinomycin D and LINC00941 RNA levels were measured by RT-qPCR at 0, 4, 8, and 12 hours. Values are normalised to the 0 h timepoint and expressed as percentage RNA remaining. Exponential decay fitting yielded half-lives of 25.7 h (control) and 5.1 h (FAM120A KD). Data are presented as mean ± SEM unless otherwise indicated. Statistical significance was determined using Student’s t -test. ∗ P < 0.05; ∗∗ P < 0.01; ∗∗∗ P < 0.001.](https://bio-rxiv-images-cdn.bioz.com/dois_ending_with_69/10__64898_slash_2026__05__11__722569/10__64898_slash_2026__05__11__722569___F3.large.jpg)