Journal: BMC Oral Health

Article Title: Wnt signaling aberrant activation drives ameloblastoma invasion and recurrence: bioinformatics and in vitro insights

doi: 10.1186/s12903-024-05003-0

Figure Lengend Snippet: The primer sequences

Article Snippet: The primary antibodies were anti-TCF7 (1:1000, Cell Signaling Technology, 2203), anti-β-catenin (1:5000, Proteintech, 66379-1-Ig), anti-WNT2B (1:1000, Affinity, DF12538), and anti-LEF1 (1:800, ZENBIO, 3382664), incubated at 4 °C for 12 h. Secondary antibodies, goat anti-rabbit (1:5000, Proteintech, SA00001-2) and goat anti-mouse (1:6000, Proteintech, SA00001-1), were incubated at room temperature for 90 min.

Techniques: Sequencing

Journal: BMC Oral Health

Article Title: Wnt signaling aberrant activation drives ameloblastoma invasion and recurrence: bioinformatics and in vitro insights

doi: 10.1186/s12903-024-05003-0

Figure Lengend Snippet: Changes in Key Gene and Protein Expression in the Wnt Pathway Under Different Concentrations of Laduviglusib. A-E : Differences in the expression of TCF7, β-catenin, WNT2B, and LEF1 proteins. F-I : Differences in mRNA expression levels of TCF7 , CTNNB1 , WNT2B , and LEF1

Article Snippet: The primary antibodies were anti-TCF7 (1:1000, Cell Signaling Technology, 2203), anti-β-catenin (1:5000, Proteintech, 66379-1-Ig), anti-WNT2B (1:1000, Affinity, DF12538), and anti-LEF1 (1:800, ZENBIO, 3382664), incubated at 4 °C for 12 h. Secondary antibodies, goat anti-rabbit (1:5000, Proteintech, SA00001-2) and goat anti-mouse (1:6000, Proteintech, SA00001-1), were incubated at room temperature for 90 min.

Techniques: Expressing

Journal: Nature Communications

Article Title: Interfering with stem cell-specific gatekeeper functions controls tumour initiation and malignant progression of skin tumours

doi: 10.1038/ncomms6874

Figure Lengend Snippet: ( a ) Architecture and marker expression within the SG of the pilosebaceous unit and lobules of sebaceous adenoma. B, bulge; BrdU, 5-bromo-2′-deoxyuridine; FASN, fatty acid synthetase; HF, hair follicle; HS, hair shaft; I, isthmus; IFE, interfollicular epidermis; JZ, junctional zone; K14, keratin 14; ORS, outer root sheath; S, sebaceous tumour lobule; SCD1, stearoyl coenzyme A desaturase; SG, sebaceous gland; str, tumour stroma. ( b ) Immunofluorescence staining of sebaceous tumour lobules of K14ΔNLef1 transgenic mice for expression of mutant Lef1 (green) and differentiation marker Adipophilin (red). ( c ) Experimental strategy to trace progeny of K15-derived bulge stem cells (BSCs) during epidermal tumorigenesis. ( d ) Detection of YFP + SCs within the bulge of deformed HF 5 days following TAM application. nSG, de novo sebaceous gland. ( e – g ) Clonal expansion of YFP + SC progeny in epidermal whole mounts of early lesions (cysts) and within the tumour lobules 42 days following DMBA treatment. ( h ) Co-localization of YFP- and SCD1 (red)-expressing cells in tumours (arrows). ( i ) Control tissue remains negative for YFP. ctrl, oil treatment. ( j ) Quantification of YFP + tumours at different stages of development and from different body sites. Scale bars, 50 μm.

Article Snippet: Following primary antibodies were used: K15 (mouse, Neomarkers, 1:1,500), K14 (rabbit, Covance, 1:3,000), K10 (rabbit, Covance, 1:500), BrdU (mouse, BD Bioscience, 1:50), BrdU (rat, Oxford Biotechnologie, 1:500), adipophilin (guinea pig, Fitzgerald Industries, 1:1,500), active Caspase-3 (rabbit, R&D Systems, 1:500), SCD1 (goat, Santa Cruz, 1:150 and rat, R&D Systems, 1:150), Lrig1 (goat, R&D Systems, 1:100), Plet1 (rat, MUbio, 1:500), E-cadherin (mouse, BD Bioscience, 1:1,000), FASN (G-11) (mouse, Santa Cruz, 1:100), Lef1 (rabbit, Cell Signaling, 1:100), γH2AX (rabbit, Cell Signaling, 1:200), p53 (rabbit, Novocastra/Leica, 1:500), p53 (mouse, Cell Signaling, 1:100) and 9E10 (rabbit, Santa Cruz, 1:200).

Techniques: Marker, Expressing, Immunofluorescence, Staining, Transgenic Assay, Mutagenesis, Derivative Assay, Control

Journal: Nature Communications

Article Title: Interfering with stem cell-specific gatekeeper functions controls tumour initiation and malignant progression of skin tumours

doi: 10.1038/ncomms6874

Figure Lengend Snippet: Expression of mutant Lef1 results in defective DNA damage response and impairment of SC-specific surveillance mechanisms, including p53 activation. SCs γH2AX carrying high levels of DNA damage undergo apoptosis, mainly by blocking the normal Bcl-2 response. Bulge SCs (BSCs) with lower degree of damaged DNA escape normal control of SC proliferation to maintain the epidermal tissue. Consequently, these proliferative SCs carrying DNA breaks accumulate further mutations, thereby initiating tumour formation.

Article Snippet: Following primary antibodies were used: K15 (mouse, Neomarkers, 1:1,500), K14 (rabbit, Covance, 1:3,000), K10 (rabbit, Covance, 1:500), BrdU (mouse, BD Bioscience, 1:50), BrdU (rat, Oxford Biotechnologie, 1:500), adipophilin (guinea pig, Fitzgerald Industries, 1:1,500), active Caspase-3 (rabbit, R&D Systems, 1:500), SCD1 (goat, Santa Cruz, 1:150 and rat, R&D Systems, 1:150), Lrig1 (goat, R&D Systems, 1:100), Plet1 (rat, MUbio, 1:500), E-cadherin (mouse, BD Bioscience, 1:1,000), FASN (G-11) (mouse, Santa Cruz, 1:100), Lef1 (rabbit, Cell Signaling, 1:100), γH2AX (rabbit, Cell Signaling, 1:200), p53 (rabbit, Novocastra/Leica, 1:500), p53 (mouse, Cell Signaling, 1:100) and 9E10 (rabbit, Santa Cruz, 1:200).

Techniques: Expressing, Mutagenesis, Activation Assay, Blocking Assay, Control