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anti nkd2 bs 1926r bioss (Bioss)

Name: anti nkd2 bs 1926r bioss
Brand: Bioss
Rating: 94 (4 reviews)

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Bioss anti nkd2 bs 1926r bioss
Anti Nkd2 Bs 1926r Bioss, supplied by Bioss, used in various techniques. Bioz Stars score: 94/100, based on 4 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Average 94 stars, based on 4 article reviews

anti nkd2 bs 1926r bioss - by Bioz Stars, 2026-02

94/100 stars

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Journal: Journal of Cellular and Molecular Medicine

Article Title: NKD2 as a Mediator of IFIX Antioncogene‐Induced Wnt Signalling and Epithelial–Mesenchymal Transition in Human OSCC

doi: 10.1111/jcmm.70342

Figure Lengend Snippet: Antibody information in IHC.

Article Snippet: Anti‐NKD2 , bs‐1926R , Bioss , 1:200.

Techniques:

Journal: Journal of Cellular and Molecular Medicine

Article Title: NKD2 as a Mediator of IFIX Antioncogene‐Induced Wnt Signalling and Epithelial–Mesenchymal Transition in Human OSCC

doi: 10.1111/jcmm.70342

Figure Lengend Snippet: Primer information.

Article Snippet: Anti‐NKD2 , bs‐1926R , Bioss , 1:200.

Techniques: Sequencing

Journal: Journal of Cellular and Molecular Medicine

Article Title: NKD2 as a Mediator of IFIX Antioncogene‐Induced Wnt Signalling and Epithelial–Mesenchymal Transition in Human OSCC

doi: 10.1111/jcmm.70342

Figure Lengend Snippet: Antibody information in WB.

Article Snippet: Anti‐NKD2 , bs‐1926R , Bioss , 1:200.

Techniques:

Journal: Journal of Cellular and Molecular Medicine

Article Title: NKD2 as a Mediator of IFIX Antioncogene‐Induced Wnt Signalling and Epithelial–Mesenchymal Transition in Human OSCC

doi: 10.1111/jcmm.70342

Figure Lengend Snippet: Antibody information in IHC.

Article Snippet: Anti‐NKD2 , bs‐1926R , Bioss , 1:200.

Techniques:

IFIX regulates Wnt signalling members including Wnt3a, Wnt4 and NKD2. (A) Western blot analysis of cell‐autonomous Wnt signalling after overexpression and knockdown of IFIX. (B) Quantification of β‐catenin expression by Western blot analysis in the CAL‐27‐vector, CAL‐27 cells (CAL‐27NC), overexpressed IFIX CAL‐27 cells (CAL‐27‐OE) and sh‐IFIX‐CAL‐27‐cells (CAL‐27‐sh). (C–F) Wnt3a and Wnt4 expression by qRT‐PCR analysis in CAL‐27 cells (CAL‐27NC), overexpressed IFIX CAL‐27 cells (CAL‐27‐OE) and Western blot analysis in CAL‐27‐vector, CAL‐27 cells (CAL‐27NC), overexpressed IFIX CAL‐27 cells (CAL‐27‐OE) and sh‐IFIX‐CAL‐27 cells (CAL‐27‐sh). (G‐H) NKD2 expression by qRT‐PCR analysis in CAL‐27 cells (CAL‐27NC), overexpressed IFIX CAL‐27 cells (CAL‐27‐OE) and Western blot analysis in the CAL‐27‐vector, CAL‐27 cells (CAL‐27NC), overexpressed IFIX CAL‐27 cells (CAL‐27‐OE) and sh‐IFIX‐CAL‐27 cells (CAL‐27‐sh). GAPDH was used as loading control. Error bars indicate mean ± SD. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

Journal: Journal of Cellular and Molecular Medicine

Article Title: NKD2 as a Mediator of IFIX Antioncogene‐Induced Wnt Signalling and Epithelial–Mesenchymal Transition in Human OSCC

doi: 10.1111/jcmm.70342

Figure Lengend Snippet: IFIX regulates Wnt signalling members including Wnt3a, Wnt4 and NKD2. (A) Western blot analysis of cell‐autonomous Wnt signalling after overexpression and knockdown of IFIX. (B) Quantification of β‐catenin expression by Western blot analysis in the CAL‐27‐vector, CAL‐27 cells (CAL‐27NC), overexpressed IFIX CAL‐27 cells (CAL‐27‐OE) and sh‐IFIX‐CAL‐27‐cells (CAL‐27‐sh). (C–F) Wnt3a and Wnt4 expression by qRT‐PCR analysis in CAL‐27 cells (CAL‐27NC), overexpressed IFIX CAL‐27 cells (CAL‐27‐OE) and Western blot analysis in CAL‐27‐vector, CAL‐27 cells (CAL‐27NC), overexpressed IFIX CAL‐27 cells (CAL‐27‐OE) and sh‐IFIX‐CAL‐27 cells (CAL‐27‐sh). (G‐H) NKD2 expression by qRT‐PCR analysis in CAL‐27 cells (CAL‐27NC), overexpressed IFIX CAL‐27 cells (CAL‐27‐OE) and Western blot analysis in the CAL‐27‐vector, CAL‐27 cells (CAL‐27NC), overexpressed IFIX CAL‐27 cells (CAL‐27‐OE) and sh‐IFIX‐CAL‐27 cells (CAL‐27‐sh). GAPDH was used as loading control. Error bars indicate mean ± SD. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

Article Snippet: Anti‐NKD2 , bs‐1926R , Bioss , 1:200.

Techniques: Western Blot, Over Expression, Knockdown, Expressing, Plasmid Preparation, Quantitative RT-PCR, Control

Silencing NKD2 induces EMT in CAL‐27 cells with overexpressed or silenced IFIX. (A) qRT‐PCR analysis quantifying NKD2 expression in CAL‐27 cells with stable expression of shRNA molecules. NKD2 expression levels in CAL‐27 cells with various treatments, including control, overexpressed IFIX (OE‐IFIX) and silenced IFIX (shIFIX), are shown. (B) Western blot analysis of NKD2 and IFIX protein levels in CAL‐27 cells with different treatments: vector control, OE‐IFIX, NC + NC, sh‐NKD2 and OE‐IFIX + sh‐NKD2. (C) Quantification of IFIX protein levels from Western blot analysis. (D) Quantification of NKD2 protein levels from Western blot analysis. (E) Western blot analysis of EMT markers (E‐cadherin, N‐cadherin, Snail and vimentin) in response to IFIX silencing by siRNA molecules in CAL‐27 cells with different treatments. (F‐I) Quantification of E‐cadherin, N‐cadherin, vimentin and Snail protein levels from Western blot analysis. Vector: OE‐IFIX CAL‐27‐vector cells; OE‐IFIX: overexpressed IFIX‐CAL‐27 cells; sh‐NKD2: Sh‐NKD2‐CAL‐27 cells; NC + NC: OE‐IFIX‐CAL‐27‐vector + sh‐NKD2 CAL‐27‐vector cells; OE‐IFIX + sh‐NKD2: OE‐IFIX + sh‐NKD2‐CAL‐27 cells. Error bars indicate mean ± SD. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

Journal: Journal of Cellular and Molecular Medicine

Article Title: NKD2 as a Mediator of IFIX Antioncogene‐Induced Wnt Signalling and Epithelial–Mesenchymal Transition in Human OSCC

doi: 10.1111/jcmm.70342

Figure Lengend Snippet: Silencing NKD2 induces EMT in CAL‐27 cells with overexpressed or silenced IFIX. (A) qRT‐PCR analysis quantifying NKD2 expression in CAL‐27 cells with stable expression of shRNA molecules. NKD2 expression levels in CAL‐27 cells with various treatments, including control, overexpressed IFIX (OE‐IFIX) and silenced IFIX (shIFIX), are shown. (B) Western blot analysis of NKD2 and IFIX protein levels in CAL‐27 cells with different treatments: vector control, OE‐IFIX, NC + NC, sh‐NKD2 and OE‐IFIX + sh‐NKD2. (C) Quantification of IFIX protein levels from Western blot analysis. (D) Quantification of NKD2 protein levels from Western blot analysis. (E) Western blot analysis of EMT markers (E‐cadherin, N‐cadherin, Snail and vimentin) in response to IFIX silencing by siRNA molecules in CAL‐27 cells with different treatments. (F‐I) Quantification of E‐cadherin, N‐cadherin, vimentin and Snail protein levels from Western blot analysis. Vector: OE‐IFIX CAL‐27‐vector cells; OE‐IFIX: overexpressed IFIX‐CAL‐27 cells; sh‐NKD2: Sh‐NKD2‐CAL‐27 cells; NC + NC: OE‐IFIX‐CAL‐27‐vector + sh‐NKD2 CAL‐27‐vector cells; OE‐IFIX + sh‐NKD2: OE‐IFIX + sh‐NKD2‐CAL‐27 cells. Error bars indicate mean ± SD. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

Article Snippet: Anti‐NKD2 , bs‐1926R , Bioss , 1:200.

Techniques: Quantitative RT-PCR, Expressing, shRNA, Control, Western Blot, Plasmid Preparation

Effects of NKD2 and IFIX on OSCC cell proliferation, migration, apoptosis and EMT in vitro. (A) Transwell assay showing the invasive ability of NC + NC‐, OE‐IFIX‐, sh‐NKD2‐ and OE‐IFIX + sh‐NKD2‐treated CAL‐27 cells. Images captured at 20× magnification. (B) Flow cytometry analysis of apoptosis in NC + NC‐, OE‐IFIX‐, sh‐NKD2‐ and OE‐IFIX + sh‐NKD2‐treated CAL‐27 cells. (C) Wound healing assay showing migration capability of NC + NC‐, OE‐IFIX‐, sh‐NKD2‐ and OE‐IFIX + sh‐NKD2‐treated CAL‐27 cells at 0 h and 48 h. Images captured at 20× magnification. (D) Quantitative analysis of invasion from the Transwell assay. Error bars indicate mean ± SD. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001. (E) Quantitative analysis of apoptosis from the flow cytometry assay. Error bars indicate mean ± SD. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001. (F) Quantitative analysis of migration from the wound healing assay. Error bars indicate mean ± SD. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001. (G) CCK‐8 assay results showing cell proliferation in NC + NC‐, OE‐IFIX‐, sh‐NKD2‐ and OE‐IFIX + sh‐NKD2‐treated CAL‐27 cells. Error bars indicate mean ± SD. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

Journal: Journal of Cellular and Molecular Medicine

Article Title: NKD2 as a Mediator of IFIX Antioncogene‐Induced Wnt Signalling and Epithelial–Mesenchymal Transition in Human OSCC

doi: 10.1111/jcmm.70342

Figure Lengend Snippet: Effects of NKD2 and IFIX on OSCC cell proliferation, migration, apoptosis and EMT in vitro. (A) Transwell assay showing the invasive ability of NC + NC‐, OE‐IFIX‐, sh‐NKD2‐ and OE‐IFIX + sh‐NKD2‐treated CAL‐27 cells. Images captured at 20× magnification. (B) Flow cytometry analysis of apoptosis in NC + NC‐, OE‐IFIX‐, sh‐NKD2‐ and OE‐IFIX + sh‐NKD2‐treated CAL‐27 cells. (C) Wound healing assay showing migration capability of NC + NC‐, OE‐IFIX‐, sh‐NKD2‐ and OE‐IFIX + sh‐NKD2‐treated CAL‐27 cells at 0 h and 48 h. Images captured at 20× magnification. (D) Quantitative analysis of invasion from the Transwell assay. Error bars indicate mean ± SD. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001. (E) Quantitative analysis of apoptosis from the flow cytometry assay. Error bars indicate mean ± SD. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001. (F) Quantitative analysis of migration from the wound healing assay. Error bars indicate mean ± SD. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001. (G) CCK‐8 assay results showing cell proliferation in NC + NC‐, OE‐IFIX‐, sh‐NKD2‐ and OE‐IFIX + sh‐NKD2‐treated CAL‐27 cells. Error bars indicate mean ± SD. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

Article Snippet: Anti‐NKD2 , bs‐1926R , Bioss , 1:200.

Techniques: Migration, In Vitro, Transwell Assay, Flow Cytometry, Wound Healing Assay, CCK-8 Assay

Effects of NKD2 and IFIX on tumour growth and EMT in vivo. (A) Tumour growth curves of SCC‐25 cells with stable expression of sh‐NKD2, OE‐IFIX, OE‐IFIX + sh‐NKD2 or NC + NC grafted into nude mice ( n = 4). Tumour volume was measured over time. Error bars indicate mean ± SD. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001. (B) Images of tumours excised from nude mice at the end of the experiment. (C) Immunohistochemistry (IHC) analysis of EMT markers (E‐cadherin, N‐cadherin, vimentin and Snail) and NKD2 expression in tumour tissues from NC + NC, sh‐NKD2, OE‐IFIX and OE‐IFIX + sh‐NKD2 groups. Images captured at 20× magnification. (D) Western blot analysis of IFIX and NKD2 protein levels in tumour tissues, with GAPDH as a loading control. (E) Quantification of tumour weights from excised tumours. Error bars indicate mean ± SD. * p < 0.05, ** p < 0.01, *** p < 0.001, ****p < 0.0001. (F) Quantification of relative protein levels of IFIX and NKD2 from Western blot analysis. Error bars indicate mean ± SD. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

Journal: Journal of Cellular and Molecular Medicine

Article Title: NKD2 as a Mediator of IFIX Antioncogene‐Induced Wnt Signalling and Epithelial–Mesenchymal Transition in Human OSCC

doi: 10.1111/jcmm.70342

Figure Lengend Snippet: Effects of NKD2 and IFIX on tumour growth and EMT in vivo. (A) Tumour growth curves of SCC‐25 cells with stable expression of sh‐NKD2, OE‐IFIX, OE‐IFIX + sh‐NKD2 or NC + NC grafted into nude mice ( n = 4). Tumour volume was measured over time. Error bars indicate mean ± SD. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001. (B) Images of tumours excised from nude mice at the end of the experiment. (C) Immunohistochemistry (IHC) analysis of EMT markers (E‐cadherin, N‐cadherin, vimentin and Snail) and NKD2 expression in tumour tissues from NC + NC, sh‐NKD2, OE‐IFIX and OE‐IFIX + sh‐NKD2 groups. Images captured at 20× magnification. (D) Western blot analysis of IFIX and NKD2 protein levels in tumour tissues, with GAPDH as a loading control. (E) Quantification of tumour weights from excised tumours. Error bars indicate mean ± SD. * p < 0.05, ** p < 0.01, *** p < 0.001, ****p < 0.0001. (F) Quantification of relative protein levels of IFIX and NKD2 from Western blot analysis. Error bars indicate mean ± SD. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

Article Snippet: Anti‐NKD2 , bs‐1926R , Bioss , 1:200.

Techniques: In Vivo, Expressing, Immunohistochemistry, Western Blot, Control

Schematic representation of IFIX regulation of the Wnt signalling pathways in OSCC. IFIX inhibits β‐catenin, affecting the canonical pathway and the expression of EMT markers. Dashed lines indicate hypothetical pathways that have not yet been experimentally confirmed. This study has demonstrated the role of IFIX in regulating NKD2 expression and its downstream effects on Wnt signalling and EMT, but further research is needed to validate these proposed interactions. Note: The roles of Frizzled, DVL and LRP5/6 in the diagram are based on established Wnt signalling pathways but were not directly investigated in this study. The hypothetical interactions (dashed lines) represent areas for future exploration to fully elucidate the mechanistic pathways involved.

Journal: Journal of Cellular and Molecular Medicine

Article Title: NKD2 as a Mediator of IFIX Antioncogene‐Induced Wnt Signalling and Epithelial–Mesenchymal Transition in Human OSCC

doi: 10.1111/jcmm.70342

Figure Lengend Snippet: Schematic representation of IFIX regulation of the Wnt signalling pathways in OSCC. IFIX inhibits β‐catenin, affecting the canonical pathway and the expression of EMT markers. Dashed lines indicate hypothetical pathways that have not yet been experimentally confirmed. This study has demonstrated the role of IFIX in regulating NKD2 expression and its downstream effects on Wnt signalling and EMT, but further research is needed to validate these proposed interactions. Note: The roles of Frizzled, DVL and LRP5/6 in the diagram are based on established Wnt signalling pathways but were not directly investigated in this study. The hypothetical interactions (dashed lines) represent areas for future exploration to fully elucidate the mechanistic pathways involved.

Article Snippet: Anti‐NKD2 , bs‐1926R , Bioss , 1:200.

Techniques: Expressing

Journal: Canadian Journal of Gastroenterology & Hepatology

Article Title: Wulingsan Alleviates MAFLD by Activating Autophagy via Regulating the AMPK/mTOR/ULK1 Signaling Pathway

doi: 10.1155/2024/9777866

Figure Lengend Snippet: Primer sequence.

Article Snippet: Antibodies against p62 (bs-2951R), ULK1 (bs-1926R), and SREBP-1c (bs-1402R) were obtained from Beijing Bioss Biotechnology Co., Ltd. (Beijing, China).

Techniques: Sequencing

Effect of WLS on regulating the AMPK/mTOR/ULK1 signaling pathway in MAFLD rats. (a–c) Hepatic p-AMPK, p-mTOR proteins expressions. (d–f) Hepatic ULK1 protein and gene expression. Results were expressed as the mean ± SD, n = 3 in (a–e) and n = 6 in (f) ∗ P < 0.05 and ∗∗ P < 0.01, compared with the model group.

Journal: Canadian Journal of Gastroenterology & Hepatology

Article Title: Wulingsan Alleviates MAFLD by Activating Autophagy via Regulating the AMPK/mTOR/ULK1 Signaling Pathway

doi: 10.1155/2024/9777866

Figure Lengend Snippet: Effect of WLS on regulating the AMPK/mTOR/ULK1 signaling pathway in MAFLD rats. (a–c) Hepatic p-AMPK, p-mTOR proteins expressions. (d–f) Hepatic ULK1 protein and gene expression. Results were expressed as the mean ± SD, n = 3 in (a–e) and n = 6 in (f) ∗ P < 0.05 and ∗∗ P < 0.01, compared with the model group.

Article Snippet: Antibodies against p62 (bs-2951R), ULK1 (bs-1926R), and SREBP-1c (bs-1402R) were obtained from Beijing Bioss Biotechnology Co., Ltd. (Beijing, China).

Techniques: Expressing

Journal: Foods

Article Title: A Comparison Study on the Therapeutic Effect of High Protein Diets Based on Pork Protein versus Soybean Protein on Obese Mice

doi: 10.3390/foods11091227

Figure Lengend Snippet: Sequences of primers in RT-qPCR.

Article Snippet: The membranes were blocked in 5% BSA prepared in 1× Tris-buffered saline with 20% Tween 20 (TBST) for 1 h. The membranes were incubated overnight with anti-PPAR-γ (bs-0530R, 1:1000), anti-UCP2 (bs-1926R, 1:1000), anti-pAMPK (bs-4002R, 1:1000), anti-pACC (bs-3039R, 1:1000), anti-AMPK (bs-2771R, 1:1000) or anti-β-actin (bs-10966R, 1:1000) antibody (Bioss, Beijing, China).

Techniques:

Effect of different protein sources on the expression of hepatic peroxisome proliferator-activated receptor-γ (PPAR-γ), uncoupling protein 2 (UCP2), phosphorylated AMP-activated protein kinase (pAMPK), and phosphorylated acetyl CoA carboxylase (pACC) in obese mice. ( A ) Effect of different proteins on hepatic PPAR-γ and UCP2 on gene expression in obese mice; ( B ) effect of different proteins on hepatic PPAR-γ, UCP2, pAMPK, and pACC on protein expression in obese mice. Different letters indicate significant differences between groups ( p < 0.05).

Journal: Foods

Article Title: A Comparison Study on the Therapeutic Effect of High Protein Diets Based on Pork Protein versus Soybean Protein on Obese Mice

doi: 10.3390/foods11091227

Figure Lengend Snippet: Effect of different protein sources on the expression of hepatic peroxisome proliferator-activated receptor-γ (PPAR-γ), uncoupling protein 2 (UCP2), phosphorylated AMP-activated protein kinase (pAMPK), and phosphorylated acetyl CoA carboxylase (pACC) in obese mice. ( A ) Effect of different proteins on hepatic PPAR-γ and UCP2 on gene expression in obese mice; ( B ) effect of different proteins on hepatic PPAR-γ, UCP2, pAMPK, and pACC on protein expression in obese mice. Different letters indicate significant differences between groups ( p < 0.05).

Techniques: Expressing

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