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The mRNA expression of <t>PIP4K2C</t> in pan-cancer. (A) The mRNA expression of PIP4K2C in 33 tumors in TCGA GTEx samples (ns, p > 0.05; * p < 0.05; ** p < 0.01; *** p < 0.001). (B) PIP4K2C expression in the breast cancer tissues and unpaired normal samples. (C) The expression level of PIP4K2C in the breast cancer tissues and the paired normal samples. ACC, adrenocortical carcinoma; BLCA, bladder urothelial carcinoma; BRCA, breast invasive carcinoma; CESC, cervical and endocervical cancers; CHOL, cholangiocarcinoma; COAD, colon adenocarcinoma; DLBC, lymphoid neoplasm diffuse large B-cell lymphoma; ESCA, esophageal carcinoma; GBM, glioblastoma multiforme; HNSC, head and neck squamous cell carcinoma; KICH, kidney chromophobe; KIRC, kidney renal clear cell carcinoma; KIRP, kidney renal papillary cell carcinoma; LAML, acute myeloid leukemia; LGG, brain lower grade glioma; LIHC, liver hepatocellular carcinoma; LUAD, lung adenocarcinoma; LUSC, lung squamous cell carcinoma; MESO, mesothelioma; OV, ovarian serous cystadenocarcinoma; PAAD, pancreatic adenocarcinoma; PCPG, pheochromocytoma and paraganglioma; PRAD, prostate adenocarcinoma; READ, rectum adenocarcinoma; SARC, sarcoma; SKCM, skin cutaneous melanoma; STAD, stomach adenocarcinoma; STES, stomach and esophageal carcinoma; TGCT, testicular germ cell tumors; THCA, thyroid carcinoma; THYM, thymoma; UCEC, uterine corpus endometrial carcinoma; UCS, uterine carcinosarcoma; UVM, uveal melanoma.
Primary Antibody Pip4k2c, supplied by Cusabio, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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The mRNA expression of <t>PIP4K2C</t> in pan-cancer. (A) The mRNA expression of PIP4K2C in 33 tumors in TCGA GTEx samples (ns, p > 0.05; * p < 0.05; ** p < 0.01; *** p < 0.001). (B) PIP4K2C expression in the breast cancer tissues and unpaired normal samples. (C) The expression level of PIP4K2C in the breast cancer tissues and the paired normal samples. ACC, adrenocortical carcinoma; BLCA, bladder urothelial carcinoma; BRCA, breast invasive carcinoma; CESC, cervical and endocervical cancers; CHOL, cholangiocarcinoma; COAD, colon adenocarcinoma; DLBC, lymphoid neoplasm diffuse large B-cell lymphoma; ESCA, esophageal carcinoma; GBM, glioblastoma multiforme; HNSC, head and neck squamous cell carcinoma; KICH, kidney chromophobe; KIRC, kidney renal clear cell carcinoma; KIRP, kidney renal papillary cell carcinoma; LAML, acute myeloid leukemia; LGG, brain lower grade glioma; LIHC, liver hepatocellular carcinoma; LUAD, lung adenocarcinoma; LUSC, lung squamous cell carcinoma; MESO, mesothelioma; OV, ovarian serous cystadenocarcinoma; PAAD, pancreatic adenocarcinoma; PCPG, pheochromocytoma and paraganglioma; PRAD, prostate adenocarcinoma; READ, rectum adenocarcinoma; SARC, sarcoma; SKCM, skin cutaneous melanoma; STAD, stomach adenocarcinoma; STES, stomach and esophageal carcinoma; TGCT, testicular germ cell tumors; THCA, thyroid carcinoma; THYM, thymoma; UCEC, uterine corpus endometrial carcinoma; UCS, uterine carcinosarcoma; UVM, uveal melanoma.
Primary Purified Polyclonal Rabbit Anti Human Hla C Antibody E Ab 17922, supplied by Elabscience Biotechnology, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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The mRNA expression of <t>PIP4K2C</t> in pan-cancer. (A) The mRNA expression of PIP4K2C in 33 tumors in TCGA GTEx samples (ns, p > 0.05; * p < 0.05; ** p < 0.01; *** p < 0.001). (B) PIP4K2C expression in the breast cancer tissues and unpaired normal samples. (C) The expression level of PIP4K2C in the breast cancer tissues and the paired normal samples. ACC, adrenocortical carcinoma; BLCA, bladder urothelial carcinoma; BRCA, breast invasive carcinoma; CESC, cervical and endocervical cancers; CHOL, cholangiocarcinoma; COAD, colon adenocarcinoma; DLBC, lymphoid neoplasm diffuse large B-cell lymphoma; ESCA, esophageal carcinoma; GBM, glioblastoma multiforme; HNSC, head and neck squamous cell carcinoma; KICH, kidney chromophobe; KIRC, kidney renal clear cell carcinoma; KIRP, kidney renal papillary cell carcinoma; LAML, acute myeloid leukemia; LGG, brain lower grade glioma; LIHC, liver hepatocellular carcinoma; LUAD, lung adenocarcinoma; LUSC, lung squamous cell carcinoma; MESO, mesothelioma; OV, ovarian serous cystadenocarcinoma; PAAD, pancreatic adenocarcinoma; PCPG, pheochromocytoma and paraganglioma; PRAD, prostate adenocarcinoma; READ, rectum adenocarcinoma; SARC, sarcoma; SKCM, skin cutaneous melanoma; STAD, stomach adenocarcinoma; STES, stomach and esophageal carcinoma; TGCT, testicular germ cell tumors; THCA, thyroid carcinoma; THYM, thymoma; UCEC, uterine corpus endometrial carcinoma; UCS, uterine carcinosarcoma; UVM, uveal melanoma.
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Novus Biologicals polyclonal rabbit anti-human cd31 primary antibody nb 100-2284
The mRNA expression of <t>PIP4K2C</t> in pan-cancer. (A) The mRNA expression of PIP4K2C in 33 tumors in TCGA GTEx samples (ns, p > 0.05; * p < 0.05; ** p < 0.01; *** p < 0.001). (B) PIP4K2C expression in the breast cancer tissues and unpaired normal samples. (C) The expression level of PIP4K2C in the breast cancer tissues and the paired normal samples. ACC, adrenocortical carcinoma; BLCA, bladder urothelial carcinoma; BRCA, breast invasive carcinoma; CESC, cervical and endocervical cancers; CHOL, cholangiocarcinoma; COAD, colon adenocarcinoma; DLBC, lymphoid neoplasm diffuse large B-cell lymphoma; ESCA, esophageal carcinoma; GBM, glioblastoma multiforme; HNSC, head and neck squamous cell carcinoma; KICH, kidney chromophobe; KIRC, kidney renal clear cell carcinoma; KIRP, kidney renal papillary cell carcinoma; LAML, acute myeloid leukemia; LGG, brain lower grade glioma; LIHC, liver hepatocellular carcinoma; LUAD, lung adenocarcinoma; LUSC, lung squamous cell carcinoma; MESO, mesothelioma; OV, ovarian serous cystadenocarcinoma; PAAD, pancreatic adenocarcinoma; PCPG, pheochromocytoma and paraganglioma; PRAD, prostate adenocarcinoma; READ, rectum adenocarcinoma; SARC, sarcoma; SKCM, skin cutaneous melanoma; STAD, stomach adenocarcinoma; STES, stomach and esophageal carcinoma; TGCT, testicular germ cell tumors; THCA, thyroid carcinoma; THYM, thymoma; UCEC, uterine corpus endometrial carcinoma; UCS, uterine carcinosarcoma; UVM, uveal melanoma.
Polyclonal Rabbit Anti Human Cd31 Primary Antibody Nb 100 2284, supplied by Novus Biologicals, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Neuronal differentiation of SH-SY5Y human neuroblastoma cells and HMGA1 and tau e xpression. ( a ) Upper panels: representative optical microscopy images of SH-SY5Y cell morphology are shown at day 1, day 5, and day 10 after starting differentiation with RA. Lower panels: representative immunofluorescence microscopy images of tau protein (green fluorescence), nuclear DAPI (blue fluorescence), and merged signals at the same time points selected for the morphological analysis of SH-SY5Y cells, during differentiation. Scale bar = 20 μm. ( b ) HMGA1 and tau mRNA and protein expression were measured in both undifferentiated (Undiff.) and differentiated (Diff.) SH-SY5Y cells, using Western blot (WB) analysis and qRT-PCR. Values represent the mean ± s.e.m. of three independent experiments. ∗∗∗ p < 0.001 versus undifferentiated cells, in each assay condition. The inset shows the progressive changes in HMGA1 and <t>INSR</t> expression over time (day 1, day 5, and day 10) following the initiation of differentiation with RA, as measured by WB. ( c ) HMGA1 and tau protein levels in the secretome of SH-SY5Y cells before and after neuronal differentiation. Left, representative WB of HMGA1 and tau in cell suspension (PBS) of undifferentiated (Undiff.) and differentiated (Diff.) SH-SY5Y cells. Ponceau S, protein loading control. Right, WB of HMGA1 in 24-h conditioned medium samples from undifferentiated (lanes 1–2) and differentiated (lanes 3–4) SH-SY5Y cells. A representative WB out of six independent experiments is shown. The absolute values of tau protein content in 24-h conditioned medium from undifferentiated (Undiff.) and differentiated (Diff.) SH-SY5Y cells are shown in bar graph (mean ± s.e.m.), together with the levels of p-tau (inset). ∗∗∗ p < 0.001 versus undifferentiated cells. ( d ) Oxidative stress in undifferentiated (Undiff.) and differentiated (Diff.) SH-SY5Y cells. Left, Representative images of the MitoSOX Red Superoxide Indicator assay, showing red fluorescence, which indicates intracellular, mitochondrial-generated superoxide, overlaid with brightfield images. Scale bar = 100 μm. Right, Quantification of reactive oxygen species (ROS) production using the ROS-Glo™ H 2 O 2 Assay. Data are expressed as mean ± s.e.m. of relative light units, normalized to the number of viable cells, from three independent experiments.
Primary Polyclonal Rabbit Anti Human Insr Antibody N 20, α Chain, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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The detailed information of antibodies used in this study.
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The detailed information of antibodies used in this study.
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The mRNA expression of PIP4K2C in pan-cancer. (A) The mRNA expression of PIP4K2C in 33 tumors in TCGA GTEx samples (ns, p > 0.05; * p < 0.05; ** p < 0.01; *** p < 0.001). (B) PIP4K2C expression in the breast cancer tissues and unpaired normal samples. (C) The expression level of PIP4K2C in the breast cancer tissues and the paired normal samples. ACC, adrenocortical carcinoma; BLCA, bladder urothelial carcinoma; BRCA, breast invasive carcinoma; CESC, cervical and endocervical cancers; CHOL, cholangiocarcinoma; COAD, colon adenocarcinoma; DLBC, lymphoid neoplasm diffuse large B-cell lymphoma; ESCA, esophageal carcinoma; GBM, glioblastoma multiforme; HNSC, head and neck squamous cell carcinoma; KICH, kidney chromophobe; KIRC, kidney renal clear cell carcinoma; KIRP, kidney renal papillary cell carcinoma; LAML, acute myeloid leukemia; LGG, brain lower grade glioma; LIHC, liver hepatocellular carcinoma; LUAD, lung adenocarcinoma; LUSC, lung squamous cell carcinoma; MESO, mesothelioma; OV, ovarian serous cystadenocarcinoma; PAAD, pancreatic adenocarcinoma; PCPG, pheochromocytoma and paraganglioma; PRAD, prostate adenocarcinoma; READ, rectum adenocarcinoma; SARC, sarcoma; SKCM, skin cutaneous melanoma; STAD, stomach adenocarcinoma; STES, stomach and esophageal carcinoma; TGCT, testicular germ cell tumors; THCA, thyroid carcinoma; THYM, thymoma; UCEC, uterine corpus endometrial carcinoma; UCS, uterine carcinosarcoma; UVM, uveal melanoma.

Journal: Translational Oncology

Article Title: Downregulation of PIP4K2C inhibits the breast cancer cell proliferation, migration and invasion

doi: 10.1016/j.tranon.2025.102420

Figure Lengend Snippet: The mRNA expression of PIP4K2C in pan-cancer. (A) The mRNA expression of PIP4K2C in 33 tumors in TCGA GTEx samples (ns, p > 0.05; * p < 0.05; ** p < 0.01; *** p < 0.001). (B) PIP4K2C expression in the breast cancer tissues and unpaired normal samples. (C) The expression level of PIP4K2C in the breast cancer tissues and the paired normal samples. ACC, adrenocortical carcinoma; BLCA, bladder urothelial carcinoma; BRCA, breast invasive carcinoma; CESC, cervical and endocervical cancers; CHOL, cholangiocarcinoma; COAD, colon adenocarcinoma; DLBC, lymphoid neoplasm diffuse large B-cell lymphoma; ESCA, esophageal carcinoma; GBM, glioblastoma multiforme; HNSC, head and neck squamous cell carcinoma; KICH, kidney chromophobe; KIRC, kidney renal clear cell carcinoma; KIRP, kidney renal papillary cell carcinoma; LAML, acute myeloid leukemia; LGG, brain lower grade glioma; LIHC, liver hepatocellular carcinoma; LUAD, lung adenocarcinoma; LUSC, lung squamous cell carcinoma; MESO, mesothelioma; OV, ovarian serous cystadenocarcinoma; PAAD, pancreatic adenocarcinoma; PCPG, pheochromocytoma and paraganglioma; PRAD, prostate adenocarcinoma; READ, rectum adenocarcinoma; SARC, sarcoma; SKCM, skin cutaneous melanoma; STAD, stomach adenocarcinoma; STES, stomach and esophageal carcinoma; TGCT, testicular germ cell tumors; THCA, thyroid carcinoma; THYM, thymoma; UCEC, uterine corpus endometrial carcinoma; UCS, uterine carcinosarcoma; UVM, uveal melanoma.

Article Snippet: In this assay, primary antibody PIP4K2C (1:100, CUSABIO, CSB-PA819455LA01HU) and secondary antibodies Goat anti-rabbit IgG H&L (Alexa Fluor® 488) (1:400, abcam, ab150077) were used.

Techniques: Expressing

mRNA expression and protein levels of PIP4K2C in breast cancer cell lines and tissues. (A) The expression level of PIP4K2C in the normal mammary gland cell line MCF-10A and breast cancer cell lines (MDA-MB-231, MDA-MB-468, MCF7, ZR751 and BT20) was determined using qPCR. * P < 0.05, *** P < 0.01 vs MCF-10A. (B) The protein levels of PIP4K2C in cell lines were measured by western blot. (C) The expression level of PIP4K2C in the breast cancer tissues and the paired normal samples. (D) The protein levels of PIP4K2C in the breast cancer tissues and the paired normal samples. (E) The immunofluorescence staining of the breast cancer tissues and the paired normal samples. (F) The IHC images of PIP4K2C in normal and tumor tissues.

Journal: Translational Oncology

Article Title: Downregulation of PIP4K2C inhibits the breast cancer cell proliferation, migration and invasion

doi: 10.1016/j.tranon.2025.102420

Figure Lengend Snippet: mRNA expression and protein levels of PIP4K2C in breast cancer cell lines and tissues. (A) The expression level of PIP4K2C in the normal mammary gland cell line MCF-10A and breast cancer cell lines (MDA-MB-231, MDA-MB-468, MCF7, ZR751 and BT20) was determined using qPCR. * P < 0.05, *** P < 0.01 vs MCF-10A. (B) The protein levels of PIP4K2C in cell lines were measured by western blot. (C) The expression level of PIP4K2C in the breast cancer tissues and the paired normal samples. (D) The protein levels of PIP4K2C in the breast cancer tissues and the paired normal samples. (E) The immunofluorescence staining of the breast cancer tissues and the paired normal samples. (F) The IHC images of PIP4K2C in normal and tumor tissues.

Article Snippet: In this assay, primary antibody PIP4K2C (1:100, CUSABIO, CSB-PA819455LA01HU) and secondary antibodies Goat anti-rabbit IgG H&L (Alexa Fluor® 488) (1:400, abcam, ab150077) were used.

Techniques: Expressing, Western Blot, Immunofluorescence, Staining

PIP4K2C was knocked down by siRNA. (A-B) The transfection efficiency of MDA-MB-468 was detected at mRNA expression and protein levels, respectively. (C-D) The transfection efficiency of MCF7 was detected at mRNA expression and protein levels (48 h), respectively.

Journal: Translational Oncology

Article Title: Downregulation of PIP4K2C inhibits the breast cancer cell proliferation, migration and invasion

doi: 10.1016/j.tranon.2025.102420

Figure Lengend Snippet: PIP4K2C was knocked down by siRNA. (A-B) The transfection efficiency of MDA-MB-468 was detected at mRNA expression and protein levels, respectively. (C-D) The transfection efficiency of MCF7 was detected at mRNA expression and protein levels (48 h), respectively.

Article Snippet: In this assay, primary antibody PIP4K2C (1:100, CUSABIO, CSB-PA819455LA01HU) and secondary antibodies Goat anti-rabbit IgG H&L (Alexa Fluor® 488) (1:400, abcam, ab150077) were used.

Techniques: Transfection, Expressing

PIP4K2C was overexpressed in MCF 10A by transfection. (A) The transfection efficiency was detected at mRNA expression. (B) overexpression of PIP4K2C resulted in increased proliferation.

Journal: Translational Oncology

Article Title: Downregulation of PIP4K2C inhibits the breast cancer cell proliferation, migration and invasion

doi: 10.1016/j.tranon.2025.102420

Figure Lengend Snippet: PIP4K2C was overexpressed in MCF 10A by transfection. (A) The transfection efficiency was detected at mRNA expression. (B) overexpression of PIP4K2C resulted in increased proliferation.

Article Snippet: In this assay, primary antibody PIP4K2C (1:100, CUSABIO, CSB-PA819455LA01HU) and secondary antibodies Goat anti-rabbit IgG H&L (Alexa Fluor® 488) (1:400, abcam, ab150077) were used.

Techniques: Transfection, Expressing, Over Expression

Inhibition of PIP4K2C suppressed the proliferation, migration and invasion of MDA-MB-468 and MCF7 cells. (A) Knockdown of PIP4K2C by siRNA resulted in reduced proliferation. (B) The reduced cell migration rate was evaluated by wound healing assay. The percentage of wound closure at 24 and 48 h was calculated using ImageJ based on the change in scratch area from time 0 h. (C-D) The cell migration and invasion ability were detected by transwell assay.

Journal: Translational Oncology

Article Title: Downregulation of PIP4K2C inhibits the breast cancer cell proliferation, migration and invasion

doi: 10.1016/j.tranon.2025.102420

Figure Lengend Snippet: Inhibition of PIP4K2C suppressed the proliferation, migration and invasion of MDA-MB-468 and MCF7 cells. (A) Knockdown of PIP4K2C by siRNA resulted in reduced proliferation. (B) The reduced cell migration rate was evaluated by wound healing assay. The percentage of wound closure at 24 and 48 h was calculated using ImageJ based on the change in scratch area from time 0 h. (C-D) The cell migration and invasion ability were detected by transwell assay.

Article Snippet: In this assay, primary antibody PIP4K2C (1:100, CUSABIO, CSB-PA819455LA01HU) and secondary antibodies Goat anti-rabbit IgG H&L (Alexa Fluor® 488) (1:400, abcam, ab150077) were used.

Techniques: Inhibition, Migration, Knockdown, Wound Healing Assay, Transwell Assay

Down-regulation of PIP4K2C enhanced the protein levels of LC3II/LC3I.

Journal: Translational Oncology

Article Title: Downregulation of PIP4K2C inhibits the breast cancer cell proliferation, migration and invasion

doi: 10.1016/j.tranon.2025.102420

Figure Lengend Snippet: Down-regulation of PIP4K2C enhanced the protein levels of LC3II/LC3I.

Article Snippet: In this assay, primary antibody PIP4K2C (1:100, CUSABIO, CSB-PA819455LA01HU) and secondary antibodies Goat anti-rabbit IgG H&L (Alexa Fluor® 488) (1:400, abcam, ab150077) were used.

Techniques:

Neuronal differentiation of SH-SY5Y human neuroblastoma cells and HMGA1 and tau e xpression. ( a ) Upper panels: representative optical microscopy images of SH-SY5Y cell morphology are shown at day 1, day 5, and day 10 after starting differentiation with RA. Lower panels: representative immunofluorescence microscopy images of tau protein (green fluorescence), nuclear DAPI (blue fluorescence), and merged signals at the same time points selected for the morphological analysis of SH-SY5Y cells, during differentiation. Scale bar = 20 μm. ( b ) HMGA1 and tau mRNA and protein expression were measured in both undifferentiated (Undiff.) and differentiated (Diff.) SH-SY5Y cells, using Western blot (WB) analysis and qRT-PCR. Values represent the mean ± s.e.m. of three independent experiments. ∗∗∗ p < 0.001 versus undifferentiated cells, in each assay condition. The inset shows the progressive changes in HMGA1 and INSR expression over time (day 1, day 5, and day 10) following the initiation of differentiation with RA, as measured by WB. ( c ) HMGA1 and tau protein levels in the secretome of SH-SY5Y cells before and after neuronal differentiation. Left, representative WB of HMGA1 and tau in cell suspension (PBS) of undifferentiated (Undiff.) and differentiated (Diff.) SH-SY5Y cells. Ponceau S, protein loading control. Right, WB of HMGA1 in 24-h conditioned medium samples from undifferentiated (lanes 1–2) and differentiated (lanes 3–4) SH-SY5Y cells. A representative WB out of six independent experiments is shown. The absolute values of tau protein content in 24-h conditioned medium from undifferentiated (Undiff.) and differentiated (Diff.) SH-SY5Y cells are shown in bar graph (mean ± s.e.m.), together with the levels of p-tau (inset). ∗∗∗ p < 0.001 versus undifferentiated cells. ( d ) Oxidative stress in undifferentiated (Undiff.) and differentiated (Diff.) SH-SY5Y cells. Left, Representative images of the MitoSOX Red Superoxide Indicator assay, showing red fluorescence, which indicates intracellular, mitochondrial-generated superoxide, overlaid with brightfield images. Scale bar = 100 μm. Right, Quantification of reactive oxygen species (ROS) production using the ROS-Glo™ H 2 O 2 Assay. Data are expressed as mean ± s.e.m. of relative light units, normalized to the number of viable cells, from three independent experiments.

Journal: eBioMedicine

Article Title: HMGA1 deficiency: a pathogenic link between tau pathology and insulin resistance

doi: 10.1016/j.ebiom.2025.105700

Figure Lengend Snippet: Neuronal differentiation of SH-SY5Y human neuroblastoma cells and HMGA1 and tau e xpression. ( a ) Upper panels: representative optical microscopy images of SH-SY5Y cell morphology are shown at day 1, day 5, and day 10 after starting differentiation with RA. Lower panels: representative immunofluorescence microscopy images of tau protein (green fluorescence), nuclear DAPI (blue fluorescence), and merged signals at the same time points selected for the morphological analysis of SH-SY5Y cells, during differentiation. Scale bar = 20 μm. ( b ) HMGA1 and tau mRNA and protein expression were measured in both undifferentiated (Undiff.) and differentiated (Diff.) SH-SY5Y cells, using Western blot (WB) analysis and qRT-PCR. Values represent the mean ± s.e.m. of three independent experiments. ∗∗∗ p < 0.001 versus undifferentiated cells, in each assay condition. The inset shows the progressive changes in HMGA1 and INSR expression over time (day 1, day 5, and day 10) following the initiation of differentiation with RA, as measured by WB. ( c ) HMGA1 and tau protein levels in the secretome of SH-SY5Y cells before and after neuronal differentiation. Left, representative WB of HMGA1 and tau in cell suspension (PBS) of undifferentiated (Undiff.) and differentiated (Diff.) SH-SY5Y cells. Ponceau S, protein loading control. Right, WB of HMGA1 in 24-h conditioned medium samples from undifferentiated (lanes 1–2) and differentiated (lanes 3–4) SH-SY5Y cells. A representative WB out of six independent experiments is shown. The absolute values of tau protein content in 24-h conditioned medium from undifferentiated (Undiff.) and differentiated (Diff.) SH-SY5Y cells are shown in bar graph (mean ± s.e.m.), together with the levels of p-tau (inset). ∗∗∗ p < 0.001 versus undifferentiated cells. ( d ) Oxidative stress in undifferentiated (Undiff.) and differentiated (Diff.) SH-SY5Y cells. Left, Representative images of the MitoSOX Red Superoxide Indicator assay, showing red fluorescence, which indicates intracellular, mitochondrial-generated superoxide, overlaid with brightfield images. Scale bar = 100 μm. Right, Quantification of reactive oxygen species (ROS) production using the ROS-Glo™ H 2 O 2 Assay. Data are expressed as mean ± s.e.m. of relative light units, normalized to the number of viable cells, from three independent experiments.

Article Snippet: For immunofluorescence assays, monocytes were fixed in glutaraldehyde, permeabilized with 0.1% Triton X-100, and incubated with primary polyclonal rabbit anti-human INSR antibody (N-20, α chain, sc-710; Santa Cruz Biotechnology; RRID: AB_631106 ) for 2 h at room temperature.

Techniques: Microscopy, Immunofluorescence, Fluorescence, Expressing, Western Blot, Quantitative RT-PCR, Suspension, Control, Generated

Hmga1, tau and InsR expression in primary cultures of mouse neurons and in Hmga1 -deficient mice . ( a ) Hmga1 and tau protein expression, as well as tau/InsR mRNA levels, were assessed in primary cultured neurons derived from wild-type mouse embryos. pcDNA3-HMGA1a expression plasmid or anti- HMGA1 siRNA (100 pmol) was transfected into cultured neurons and Hmga1 protein and tau/InsR mRNA were measured 48–96 h later. ∗ p < 0.05, ∗∗ p < 0.01 versus control siRNA-transfected cells. Data are shown as the mean ± s.e.m. of three independent experiments. ( b ) Hmga1, InsR and tau mRNA and protein expression (left) in cerebral tissues from wild-type (+/+) and Hmga1 knockout (−/−) mice. mRNA was measured by qRT-PCR and normalized to Rps9 . Data from three independent assays from six animals per genotype are shown, together with representative Western blots (WB) of Hmga1, tau and p-tau (p-Tau1, Ser400/Thr403/Ser404; and p-Tau2, Thr205) (right) along with densitometric analysis of the blots. ∗∗ p < 0.01, ∗∗∗ p < 0.001 versus wild-type mice.

Journal: eBioMedicine

Article Title: HMGA1 deficiency: a pathogenic link between tau pathology and insulin resistance

doi: 10.1016/j.ebiom.2025.105700

Figure Lengend Snippet: Hmga1, tau and InsR expression in primary cultures of mouse neurons and in Hmga1 -deficient mice . ( a ) Hmga1 and tau protein expression, as well as tau/InsR mRNA levels, were assessed in primary cultured neurons derived from wild-type mouse embryos. pcDNA3-HMGA1a expression plasmid or anti- HMGA1 siRNA (100 pmol) was transfected into cultured neurons and Hmga1 protein and tau/InsR mRNA were measured 48–96 h later. ∗ p < 0.05, ∗∗ p < 0.01 versus control siRNA-transfected cells. Data are shown as the mean ± s.e.m. of three independent experiments. ( b ) Hmga1, InsR and tau mRNA and protein expression (left) in cerebral tissues from wild-type (+/+) and Hmga1 knockout (−/−) mice. mRNA was measured by qRT-PCR and normalized to Rps9 . Data from three independent assays from six animals per genotype are shown, together with representative Western blots (WB) of Hmga1, tau and p-tau (p-Tau1, Ser400/Thr403/Ser404; and p-Tau2, Thr205) (right) along with densitometric analysis of the blots. ∗∗ p < 0.01, ∗∗∗ p < 0.001 versus wild-type mice.

Article Snippet: For immunofluorescence assays, monocytes were fixed in glutaraldehyde, permeabilized with 0.1% Triton X-100, and incubated with primary polyclonal rabbit anti-human INSR antibody (N-20, α chain, sc-710; Santa Cruz Biotechnology; RRID: AB_631106 ) for 2 h at room temperature.

Techniques: Expressing, Cell Culture, Derivative Assay, Plasmid Preparation, Transfection, Control, Knock-Out, Quantitative RT-PCR, Western Blot

INSR expression and insulin binding in circulating blood monocytes. ( a ) Immunofluorescence of blood monocytes from AD patients, with and without the rs146052672 variant, fixed and stained with anti-INSR antibody. Representative immunofluorescence microscopy images of cell surface INSR protein (green fluorescence), nuclear DAPI (blue fluorescence), and merged signals. Scale bar = 2 μm. ( b ) Left: biotinylated insulin (B-Insulin) binding to the INSR was measured in intact monocytes from AD patients carrying (n = 6) or not carrying (n = 12) the HMGA1 variant. Fluorescence intensities are shown in bar graph (mean ± s.e.m.) for each HMGA1 genotype. Right, INSR expression was measured in monocytes from wild-type AD patient (n = 12) and AD variant carriers (n = 6), by Western blot (WB) analysis. A representative blot is shown, together with densitometric values (mean ± s.e.m). ∗∗ p < 0.01, ∗∗∗ p < 0.001.

Journal: eBioMedicine

Article Title: HMGA1 deficiency: a pathogenic link between tau pathology and insulin resistance

doi: 10.1016/j.ebiom.2025.105700

Figure Lengend Snippet: INSR expression and insulin binding in circulating blood monocytes. ( a ) Immunofluorescence of blood monocytes from AD patients, with and without the rs146052672 variant, fixed and stained with anti-INSR antibody. Representative immunofluorescence microscopy images of cell surface INSR protein (green fluorescence), nuclear DAPI (blue fluorescence), and merged signals. Scale bar = 2 μm. ( b ) Left: biotinylated insulin (B-Insulin) binding to the INSR was measured in intact monocytes from AD patients carrying (n = 6) or not carrying (n = 12) the HMGA1 variant. Fluorescence intensities are shown in bar graph (mean ± s.e.m.) for each HMGA1 genotype. Right, INSR expression was measured in monocytes from wild-type AD patient (n = 12) and AD variant carriers (n = 6), by Western blot (WB) analysis. A representative blot is shown, together with densitometric values (mean ± s.e.m). ∗∗ p < 0.01, ∗∗∗ p < 0.001.

Article Snippet: For immunofluorescence assays, monocytes were fixed in glutaraldehyde, permeabilized with 0.1% Triton X-100, and incubated with primary polyclonal rabbit anti-human INSR antibody (N-20, α chain, sc-710; Santa Cruz Biotechnology; RRID: AB_631106 ) for 2 h at room temperature.

Techniques: Expressing, Binding Assay, Immunofluorescence, Variant Assay, Staining, Microscopy, Fluorescence, Western Blot

The detailed information of antibodies used in this study.

Journal: Scientific Reports

Article Title: Impact of LIN7A silencing on U87 cell invasion and its clinical significance in glioblastoma

doi: 10.1038/s41598-025-91285-5

Figure Lengend Snippet: The detailed information of antibodies used in this study.

Article Snippet: Primary antibody , Anti-human nestin (rabbit polyclonal) , IF 1:200 , ZRB69 , MilliporeSigma.

Techniques: