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Medion Diagnostics diff-quick staining kit
Diff Quick Staining Kit, supplied by Medion Diagnostics, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/diff+quick+kit/diff+quick+staining+kit/pmc03754214-126-5-8
Average 90 stars, based on 1 article reviews
diff-quick staining kit - by Bioz Stars, 2026-11
90/100 stars

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Diff-Quik:

Article Title: The Role of Testosterone in Spermatogenesis: Lessons From Proteome Profiling of Human Spermatozoa in Testosterone Deficiency
Article Snippet: .. For Diff-Quick staining, sperm smears were prepared by placing 5 μl of the sample onto a slide and pulling it out into a smear using a second slide followed by air drying for 20–30 s. The staining kit used was Diff-Quick (Medion Diagnostics AG, Düdingen, Switzerland), and smears were stained according to the manufacturer’s instructions. .. For sperm RNA analysis, sperm RNA was individually extracted and purified following the RNeasy Mini Kit protocol (Qiagen, Hilden, Germany) with some modifications previously established ( ).

Article Title: Partially Hydrolysed Whey-Based Infant Formula Improves Skin Barrier Function
Article Snippet: .. Cell pellets were suspended in 150 μL of PBS and 0.2% BSA and transferred on slides by cytospin for 5 min at 500 g. Cells were stained using the DIFF Quick staining kit (Medion Diagnostics, Miami, FL, USA) following the manufacturer’s instructions to differentiate cell types and quantified. .. Total IgE levels were quantified by ELISA (BD Biosciences, Allschwil, Switzerland) following the manufacturer’s protocol.

Article Title: 3, 3′- (3, 5-DCPBC) Down-Regulates Multiple Phosphokinase Dependent Signal Transduction Pathways in Malignant Melanoma Cells through Specific Diminution of EGFR Y1086 Phosphorylation
Article Snippet: Thiazolyl blue tetrazolium bromide (MTT) dye, #M655, Accutase solution, (#A6964), Human placental type-IV collagen (#C5533), and DMSO (#276855) were purchased from Sigma Aldrich GmbH. .. Diff Quick staining solution kit (#B4132-1A) was purchased from Medion Diagnostic AG, Bern, Switzerland. .. Primary antibodies: anti-BrdU antibody #555627 was purchased from BD Biosciences, Waltham, MA, USA.

Staining:

Article Title: The Role of Testosterone in Spermatogenesis: Lessons From Proteome Profiling of Human Spermatozoa in Testosterone Deficiency
Article Snippet: .. For Diff-Quick staining, sperm smears were prepared by placing 5 μl of the sample onto a slide and pulling it out into a smear using a second slide followed by air drying for 20–30 s. The staining kit used was Diff-Quick (Medion Diagnostics AG, Düdingen, Switzerland), and smears were stained according to the manufacturer’s instructions. .. For sperm RNA analysis, sperm RNA was individually extracted and purified following the RNeasy Mini Kit protocol (Qiagen, Hilden, Germany) with some modifications previously established ( ).

Article Title: Partially Hydrolysed Whey-Based Infant Formula Improves Skin Barrier Function
Article Snippet: .. Cell pellets were suspended in 150 μL of PBS and 0.2% BSA and transferred on slides by cytospin for 5 min at 500 g. Cells were stained using the DIFF Quick staining kit (Medion Diagnostics, Miami, FL, USA) following the manufacturer’s instructions to differentiate cell types and quantified. .. Total IgE levels were quantified by ELISA (BD Biosciences, Allschwil, Switzerland) following the manufacturer’s protocol.

Article Title: 3, 3′- (3, 5-DCPBC) Down-Regulates Multiple Phosphokinase Dependent Signal Transduction Pathways in Malignant Melanoma Cells through Specific Diminution of EGFR Y1086 Phosphorylation
Article Snippet: Thiazolyl blue tetrazolium bromide (MTT) dye, #M655, Accutase solution, (#A6964), Human placental type-IV collagen (#C5533), and DMSO (#276855) were purchased from Sigma Aldrich GmbH. .. Diff Quick staining solution kit (#B4132-1A) was purchased from Medion Diagnostic AG, Bern, Switzerland. .. Primary antibodies: anti-BrdU antibody #555627 was purchased from BD Biosciences, Waltham, MA, USA.

other:

Article Title: Dermal fibroblast-to-myofibroblast transition sustained by αvß3 integrin-ILK-Snail1/Slug signaling is a common feature for hypermobile Ehlers-Danlos syndrome and hypermobility spectrum disorders.
Article Snippet: Migrated cells collected in the bottom chamber were methanol-fixed and stained with Diff-Quick staining kit (Medion Diagnostic GmbH, Switzerland), following manufacturer’s instructions.

Article Title: Calmodulin downregulation in conditional knockout HeLa cells inhibits cell migration.
Article Snippet: This is a PDF file of an article that has undergone enhancements after acceptance, such as the addition of a cover page and metadata, and formatting for readability, but it is not yet the definitive version of record.. This version will undergo additional copyediting, typesetting and review before it is published in its final form, but we are providing this version to give early visibility of the article.. Please note that, during the production process, errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.

Article Title: Temporal inhibition of mouse mammary gland cancer metastasis by CORM-A1 and DETA/NO combination therapy.
Article Snippet: Migrated cells on the undersides of the insert membranes were fixed and stained using Diff-Quick Stain kit (Medion Diagnostics, Miami, USA).

Article Title: Increased susceptibility to diet-induced obesity in female mice impairs ovarian steroidogenesis: The role of elevated leptin signalling on nodal activity inhibition in theca cells.
Article Snippet: Vaginal lavage was performed using saline, and the collected smears were placed on slides and stained with the Diff-Quick Staining Set (Diff- Quick Color Kit, Rapid Staining Set, Medion Grifols Diagnostics AG, Duedingen, Switzerland) for cell identification [48].



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RBM23 knockdown inhibits colon cancer cell growth and survival (A) Protein was extracted from the normal colon cell lines CCD-18Co and colon cancer cell lines (HCT116, HT29, LOVO, LS513, DLD-1, COLO205, HCT15) and quantified in equal amounts, and then the protein expression of RBM23 was detected by western blotting. (B) The mRNA expression level of RBM23 was measured by qRT-PCR in the normal colon cell line CCD-18Co and colon cancer cell lines (DLD-1, HCT15, HT29, HCT116). GAPDH was used as an internal control for normalization. (C) Western blot analysis was performed to measure the expression levels of c-Myc in HCT15 cells treated with control siRNA or RBM23 siRNA for 72 h. (D) HCT116 cells were treated with control siRNA or RBM23 siRNA #1, #2, #3 for 72 h. Protein expression levels of various factors were then analyzed by western blotting. (E) The effect of RBM23 deficiency on HCT116, a colon cancer cell line. HCT116 was transfected with 80 nM RBM23 siRNA and control siRNA, and cell viability was examined at 0 and 72 h of treatment. Cell viability was measured by CCK8 assay and optical density was measured by microplate reader at 450 nm. Data were normalized to the control siRNA group at 0 h (set as 100%). (F) The effect of RBM23 knockdown in colon cancer cells, HCT116, on cell proliferation. HCT116 cells were transfected with RBM23 siRNA (100 nM) and incubated for one week, and colonies were stained with <t>Diff</t> <t>Quick</t> solution. The colonies were counted and quantified. (G) Western blotting was performed to detect proteins extracted from HCT116 cells fractionated into nucleus and cytoplasm. Proteins from HCT116 cells transfected with RBM23 siRNA (100 nM) for 72 h were extracted and separated by NE-PER nuclear and cytoplasmic extraction kit into proteins extracted from the nucleus and cytoplasm. The proteins were then detected using western blotting. Student’s t -test: ***P < 0.001
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RBM23 knockdown inhibits colon cancer cell growth and survival (A) Protein was extracted from the normal colon cell lines CCD-18Co and colon cancer cell lines (HCT116, HT29, LOVO, LS513, DLD-1, COLO205, HCT15) and quantified in equal amounts, and then the protein expression of RBM23 was detected by western blotting. (B) The mRNA expression level of RBM23 was measured by qRT-PCR in the normal colon cell line CCD-18Co and colon cancer cell lines (DLD-1, HCT15, HT29, HCT116). GAPDH was used as an internal control for normalization. (C) Western blot analysis was performed to measure the expression levels of c-Myc in HCT15 cells treated with control siRNA or RBM23 siRNA for 72 h. (D) HCT116 cells were treated with control siRNA or RBM23 siRNA #1, #2, #3 for 72 h. Protein expression levels of various factors were then analyzed by western blotting. (E) The effect of RBM23 deficiency on HCT116, a colon cancer cell line. HCT116 was transfected with 80 nM RBM23 siRNA and control siRNA, and cell viability was examined at 0 and 72 h of treatment. Cell viability was measured by CCK8 assay and optical density was measured by microplate reader at 450 nm. Data were normalized to the control siRNA group at 0 h (set as 100%). (F) The effect of RBM23 knockdown in colon cancer cells, HCT116, on cell proliferation. HCT116 cells were transfected with RBM23 siRNA (100 nM) and incubated for one week, and colonies were stained with <t>Diff</t> <t>Quick</t> solution. The colonies were counted and quantified. (G) Western blotting was performed to detect proteins extracted from HCT116 cells fractionated into nucleus and cytoplasm. Proteins from HCT116 cells transfected with RBM23 siRNA (100 nM) for 72 h were extracted and separated by NE-PER nuclear and cytoplasmic extraction kit into proteins extracted from the nucleus and cytoplasm. The proteins were then detected using western blotting. Student’s t -test: ***P < 0.001
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RBM23 knockdown inhibits colon cancer cell growth and survival (A) Protein was extracted from the normal colon cell lines CCD-18Co and colon cancer cell lines (HCT116, HT29, LOVO, LS513, DLD-1, COLO205, HCT15) and quantified in equal amounts, and then the protein expression of RBM23 was detected by western blotting. (B) The mRNA expression level of RBM23 was measured by qRT-PCR in the normal colon cell line CCD-18Co and colon cancer cell lines (DLD-1, HCT15, HT29, HCT116). GAPDH was used as an internal control for normalization. (C) Western blot analysis was performed to measure the expression levels of c-Myc in HCT15 cells treated with control siRNA or RBM23 siRNA for 72 h. (D) HCT116 cells were treated with control siRNA or RBM23 siRNA #1, #2, #3 for 72 h. Protein expression levels of various factors were then analyzed by western blotting. (E) The effect of RBM23 deficiency on HCT116, a colon cancer cell line. HCT116 was transfected with 80 nM RBM23 siRNA and control siRNA, and cell viability was examined at 0 and 72 h of treatment. Cell viability was measured by CCK8 assay and optical density was measured by microplate reader at 450 nm. Data were normalized to the control siRNA group at 0 h (set as 100%). (F) The effect of RBM23 knockdown in colon cancer cells, HCT116, on cell proliferation. HCT116 cells were transfected with RBM23 siRNA (100 nM) and incubated for one week, and colonies were stained with <t>Diff</t> <t>Quick</t> solution. The colonies were counted and quantified. (G) Western blotting was performed to detect proteins extracted from HCT116 cells fractionated into nucleus and cytoplasm. Proteins from HCT116 cells transfected with RBM23 siRNA (100 nM) for 72 h were extracted and separated by NE-PER nuclear and cytoplasmic extraction kit into proteins extracted from the nucleus and cytoplasm. The proteins were then detected using western blotting. Student’s t -test: ***P < 0.001
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RBM23 knockdown inhibits colon cancer cell growth and survival (A) Protein was extracted from the normal colon cell lines CCD-18Co and colon cancer cell lines (HCT116, HT29, LOVO, LS513, DLD-1, COLO205, HCT15) and quantified in equal amounts, and then the protein expression of RBM23 was detected by western blotting. (B) The mRNA expression level of RBM23 was measured by qRT-PCR in the normal colon cell line CCD-18Co and colon cancer cell lines (DLD-1, HCT15, HT29, HCT116). GAPDH was used as an internal control for normalization. (C) Western blot analysis was performed to measure the expression levels of c-Myc in HCT15 cells treated with control siRNA or RBM23 siRNA for 72 h. (D) HCT116 cells were treated with control siRNA or RBM23 siRNA #1, #2, #3 for 72 h. Protein expression levels of various factors were then analyzed by western blotting. (E) The effect of RBM23 deficiency on HCT116, a colon cancer cell line. HCT116 was transfected with 80 nM RBM23 siRNA and control siRNA, and cell viability was examined at 0 and 72 h of treatment. Cell viability was measured by CCK8 assay and optical density was measured by microplate reader at 450 nm. Data were normalized to the control siRNA group at 0 h (set as 100%). (F) The effect of RBM23 knockdown in colon cancer cells, HCT116, on cell proliferation. HCT116 cells were transfected with RBM23 siRNA (100 nM) and incubated for one week, and colonies were stained with Diff Quick solution. The colonies were counted and quantified. (G) Western blotting was performed to detect proteins extracted from HCT116 cells fractionated into nucleus and cytoplasm. Proteins from HCT116 cells transfected with RBM23 siRNA (100 nM) for 72 h were extracted and separated by NE-PER nuclear and cytoplasmic extraction kit into proteins extracted from the nucleus and cytoplasm. The proteins were then detected using western blotting. Student’s t -test: ***P < 0.001

Journal: Cancer Cell International

Article Title: Inhibition of RBM23 induces ferroptosis in colon cancer cells via c-Myc regulation

doi: 10.1186/s12935-026-04262-x

Figure Lengend Snippet: RBM23 knockdown inhibits colon cancer cell growth and survival (A) Protein was extracted from the normal colon cell lines CCD-18Co and colon cancer cell lines (HCT116, HT29, LOVO, LS513, DLD-1, COLO205, HCT15) and quantified in equal amounts, and then the protein expression of RBM23 was detected by western blotting. (B) The mRNA expression level of RBM23 was measured by qRT-PCR in the normal colon cell line CCD-18Co and colon cancer cell lines (DLD-1, HCT15, HT29, HCT116). GAPDH was used as an internal control for normalization. (C) Western blot analysis was performed to measure the expression levels of c-Myc in HCT15 cells treated with control siRNA or RBM23 siRNA for 72 h. (D) HCT116 cells were treated with control siRNA or RBM23 siRNA #1, #2, #3 for 72 h. Protein expression levels of various factors were then analyzed by western blotting. (E) The effect of RBM23 deficiency on HCT116, a colon cancer cell line. HCT116 was transfected with 80 nM RBM23 siRNA and control siRNA, and cell viability was examined at 0 and 72 h of treatment. Cell viability was measured by CCK8 assay and optical density was measured by microplate reader at 450 nm. Data were normalized to the control siRNA group at 0 h (set as 100%). (F) The effect of RBM23 knockdown in colon cancer cells, HCT116, on cell proliferation. HCT116 cells were transfected with RBM23 siRNA (100 nM) and incubated for one week, and colonies were stained with Diff Quick solution. The colonies were counted and quantified. (G) Western blotting was performed to detect proteins extracted from HCT116 cells fractionated into nucleus and cytoplasm. Proteins from HCT116 cells transfected with RBM23 siRNA (100 nM) for 72 h were extracted and separated by NE-PER nuclear and cytoplasmic extraction kit into proteins extracted from the nucleus and cytoplasm. The proteins were then detected using western blotting. Student’s t -test: ***P < 0.001

Article Snippet: The plates were then incubated at 37 °C, 5% CO 2 for 1 week and the colonies were fixed and stained using Diff-Quick Kit (Sysmex Corporation, Kobe, Hyogo, Japan) and the number of colonies was counted.

Techniques: Knockdown, Expressing, Western Blot, Quantitative RT-PCR, Control, Transfection, CCK-8 Assay, Incubation, Staining, Diff-Quik, Extraction