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Overexpression of CRAF activates the RAF/MEK/ERK signaling pathway. Reverse transcription-quantitative PCR was used to analyze the mRNA expression of (A) ARAF, (B) <t>BRAF,</t> (C) CRAF, (D) MEK1, (E) MEK2, (F) ERK1and (G) ERK2. Western blotting was used to analyze the protein levels of (H) ARAF, (I) BRAF, (J) CRAF, (K) MEK1/2, (L) p-MEK1/2, (M) p-MEK1/2 to MEK1/2, (N) ERK1/2, (O) p-ERK1/2 and (P) p-ERK1/2 to ERK1/2. *P<0.05, **P<0.01 and ***P<0.001. p-, phosphorylated; OE, overexpression; NC, negative control; sh, short hairpin; ns, not significant; ARAF, <t>A-Raf</t> <t>proto-oncogene</t> <t>serine/threonine-protein</t> kinase; <t>BRAF,</t> <t>B-Raf</t> proto-oncogene serine/threonine-protein kinase; CRAF, C-Raf proto-oncogene serine/threonine-protein kinase.
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MedChemExpress recombinant igfbp2 protein
Neuron-specific <t>Igfbp2</t> deficiency in the PFC induces cognitive dysfunction (A) Schematic of the experimental design. (B) Diagram of viral injection into the PFC (top) and representative image of viral expression (bottom); scale bars, 500 μm. (C) Representative western blot bands (top) and quantification of Igfbp2 protein levels in the PFC (bottom); n = 4 mice per group. (D) Schematic of the novel object recognition test, depicting the training phase (top) and the test phase (bottom). (E) Representative trajectory plots from the novel object recognition test. (F) Quantification of time spent investigating the novel object during the test phase; n = 8 mice per group. (G) Quantification of the number of investigations of the novel object during the test phase; n = 8 mice per group. (H) Schematic of the Y-maze test, depicting the training phase (top) and the test phase (bottom). (I) Representative trajectory plots from the Y-maze test. (J) Quantification of time spent in the novel arm during the test phase; n = 8 mice per group. (K) Quantification of the number of entries into the novel arm during the test phase; n = 8 mice per group. Analyzed by unpaired t test; ∗∗ p < 0.01. Data are presented as means ± SEM.
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Overexpression of CRAF activates the RAF/MEK/ERK signaling pathway. Reverse transcription-quantitative PCR was used to analyze the mRNA expression of (A) ARAF, (B) BRAF, (C) CRAF, (D) MEK1, (E) MEK2, (F) ERK1and (G) ERK2. Western blotting was used to analyze the protein levels of (H) ARAF, (I) BRAF, (J) CRAF, (K) MEK1/2, (L) p-MEK1/2, (M) p-MEK1/2 to MEK1/2, (N) ERK1/2, (O) p-ERK1/2 and (P) p-ERK1/2 to ERK1/2. *P<0.05, **P<0.01 and ***P<0.001. p-, phosphorylated; OE, overexpression; NC, negative control; sh, short hairpin; ns, not significant; ARAF, A-Raf proto-oncogene serine/threonine-protein kinase; BRAF, B-Raf proto-oncogene serine/threonine-protein kinase; CRAF, C-Raf proto-oncogene serine/threonine-protein kinase.

Journal: Molecular Medicine Reports

Article Title: RUVBL1 and CRAF promote periodontal ligament stem cell osteogenic differentiation via the MEK/ERK signaling cascade

doi: 10.3892/mmr.2026.13881

Figure Lengend Snippet: Overexpression of CRAF activates the RAF/MEK/ERK signaling pathway. Reverse transcription-quantitative PCR was used to analyze the mRNA expression of (A) ARAF, (B) BRAF, (C) CRAF, (D) MEK1, (E) MEK2, (F) ERK1and (G) ERK2. Western blotting was used to analyze the protein levels of (H) ARAF, (I) BRAF, (J) CRAF, (K) MEK1/2, (L) p-MEK1/2, (M) p-MEK1/2 to MEK1/2, (N) ERK1/2, (O) p-ERK1/2 and (P) p-ERK1/2 to ERK1/2. *P<0.05, **P<0.01 and ***P<0.001. p-, phosphorylated; OE, overexpression; NC, negative control; sh, short hairpin; ns, not significant; ARAF, A-Raf proto-oncogene serine/threonine-protein kinase; BRAF, B-Raf proto-oncogene serine/threonine-protein kinase; CRAF, C-Raf proto-oncogene serine/threonine-protein kinase.

Article Snippet: The antibodies were as follows: GAPDH (1:1,000; cat. no. P30008M; Abmart Pharmaceutical Technology Co., Ltd.), A-Raf proto-oncogene serine/threonine-protein kinase (ARAF) (cat. no. bs-2251R), CRAF (cat. no. bs-23170R), MEK1/2 (cat. no. bs-1041R), phosphorylated (p)-MEK1/2 (cat. no. bs-3270R), ERK1/2 (cat. no. bsm-33232M), p-ERK1/2 (cat. no. bs-3016R; all BIOSS), RUVBL1 (cat. no. 74775; Cell Signaling Technology, Inc.), ERK1/2 (all 1:500; cat. no. bsm-33232M; BIOSS), B-Raf proto-oncogene serine/threonine-protein kinase (BRAF) (1:2,000; cat. no. ab33899; Abcam) and HRP-conjugated universal secondary antibody [cat. nos.

Techniques: Over Expression, Reverse Transcription, Real-time Polymerase Chain Reaction, Expressing, Western Blot, Negative Control

Overexpression of RUVBL1 activates the MEK/ERK signaling pathway. Reverse transcription-quantitative PCR was used to analyze the mRNA expression of (A) ARAF, (B) BRAF, (C) CRAF, (D) MEK1, (E) MEK2, (F) ERK1 and (G) ERK2. Western blotting was used to analyze protein levels of (H) ARAF, (I) BRAF, (J) CRAF, (K) MEK1/2, (L) p-MEK1/2, (M) p-MEK1/2 to MEK1/2, (N) ERK1/2, (O) p-ERK1/2 and (P) p-ERK1/2 to ERK1/2. *P<0.05, **P<0.01 and ***P<0.001. RUVBL1, RuvB-like AAA ATPase-1; p-, phosphorylated; OE, overexpression; NC, negative control; sh, short hairpin; ns, not significant; ARAF, A-Raf proto-oncogene serine/threonine-protein kinase; BRAF, B-Raf proto-oncogene serine/threonine-protein kinase; CRAF, C-Raf proto-oncogene serine/threonine-protein kinase.

Journal: Molecular Medicine Reports

Article Title: RUVBL1 and CRAF promote periodontal ligament stem cell osteogenic differentiation via the MEK/ERK signaling cascade

doi: 10.3892/mmr.2026.13881

Figure Lengend Snippet: Overexpression of RUVBL1 activates the MEK/ERK signaling pathway. Reverse transcription-quantitative PCR was used to analyze the mRNA expression of (A) ARAF, (B) BRAF, (C) CRAF, (D) MEK1, (E) MEK2, (F) ERK1 and (G) ERK2. Western blotting was used to analyze protein levels of (H) ARAF, (I) BRAF, (J) CRAF, (K) MEK1/2, (L) p-MEK1/2, (M) p-MEK1/2 to MEK1/2, (N) ERK1/2, (O) p-ERK1/2 and (P) p-ERK1/2 to ERK1/2. *P<0.05, **P<0.01 and ***P<0.001. RUVBL1, RuvB-like AAA ATPase-1; p-, phosphorylated; OE, overexpression; NC, negative control; sh, short hairpin; ns, not significant; ARAF, A-Raf proto-oncogene serine/threonine-protein kinase; BRAF, B-Raf proto-oncogene serine/threonine-protein kinase; CRAF, C-Raf proto-oncogene serine/threonine-protein kinase.

Article Snippet: The antibodies were as follows: GAPDH (1:1,000; cat. no. P30008M; Abmart Pharmaceutical Technology Co., Ltd.), A-Raf proto-oncogene serine/threonine-protein kinase (ARAF) (cat. no. bs-2251R), CRAF (cat. no. bs-23170R), MEK1/2 (cat. no. bs-1041R), phosphorylated (p)-MEK1/2 (cat. no. bs-3270R), ERK1/2 (cat. no. bsm-33232M), p-ERK1/2 (cat. no. bs-3016R; all BIOSS), RUVBL1 (cat. no. 74775; Cell Signaling Technology, Inc.), ERK1/2 (all 1:500; cat. no. bsm-33232M; BIOSS), B-Raf proto-oncogene serine/threonine-protein kinase (BRAF) (1:2,000; cat. no. ab33899; Abcam) and HRP-conjugated universal secondary antibody [cat. nos.

Techniques: Over Expression, Reverse Transcription, Real-time Polymerase Chain Reaction, Expressing, Western Blot, Negative Control

ODN MT01 promotes osteogenic differentiation of PDLSCs. (A) PDLSC proliferation and (B) ALP staining following treatment with varying concentrations of ODN MT01. (C) Osteogenic differentiation and (D) mineralization after the addition of ODN MT01 and osteogenic inducers. ALP staining was used to assess the effect of (E) CRAF and (F) RUVBL1 on osteogenic differentiation of PDLSCs following the addition of ODN MT01 and osteogenic inducers. Alizarin Red staining was used to assess the effect of (G) CRAF and (H) RUVBL1 on the degree of mineralization of PDLSCs following the addition of ODN MT01 and osteogenic inducers. *P<0.05 and ***P<0.001. ODN, oligodeoxynucleotide; PDLSC, periodontal ligament stem cell; ALP, alkaline phosphatase, RUVBL1, RuvB-like AAA ATPase-1; NC, negative control; OE, overexpression; sh, short hairpin; ns, not significant; CRAF, C-Raf proto-oncogene serine/threonine-protein kinase; OI, osteogenic induction; OM, ODN MT01.

Journal: Molecular Medicine Reports

Article Title: RUVBL1 and CRAF promote periodontal ligament stem cell osteogenic differentiation via the MEK/ERK signaling cascade

doi: 10.3892/mmr.2026.13881

Figure Lengend Snippet: ODN MT01 promotes osteogenic differentiation of PDLSCs. (A) PDLSC proliferation and (B) ALP staining following treatment with varying concentrations of ODN MT01. (C) Osteogenic differentiation and (D) mineralization after the addition of ODN MT01 and osteogenic inducers. ALP staining was used to assess the effect of (E) CRAF and (F) RUVBL1 on osteogenic differentiation of PDLSCs following the addition of ODN MT01 and osteogenic inducers. Alizarin Red staining was used to assess the effect of (G) CRAF and (H) RUVBL1 on the degree of mineralization of PDLSCs following the addition of ODN MT01 and osteogenic inducers. *P<0.05 and ***P<0.001. ODN, oligodeoxynucleotide; PDLSC, periodontal ligament stem cell; ALP, alkaline phosphatase, RUVBL1, RuvB-like AAA ATPase-1; NC, negative control; OE, overexpression; sh, short hairpin; ns, not significant; CRAF, C-Raf proto-oncogene serine/threonine-protein kinase; OI, osteogenic induction; OM, ODN MT01.

Article Snippet: The antibodies were as follows: GAPDH (1:1,000; cat. no. P30008M; Abmart Pharmaceutical Technology Co., Ltd.), A-Raf proto-oncogene serine/threonine-protein kinase (ARAF) (cat. no. bs-2251R), CRAF (cat. no. bs-23170R), MEK1/2 (cat. no. bs-1041R), phosphorylated (p)-MEK1/2 (cat. no. bs-3270R), ERK1/2 (cat. no. bsm-33232M), p-ERK1/2 (cat. no. bs-3016R; all BIOSS), RUVBL1 (cat. no. 74775; Cell Signaling Technology, Inc.), ERK1/2 (all 1:500; cat. no. bsm-33232M; BIOSS), B-Raf proto-oncogene serine/threonine-protein kinase (BRAF) (1:2,000; cat. no. ab33899; Abcam) and HRP-conjugated universal secondary antibody [cat. nos.

Techniques: Staining, Negative Control, Over Expression

Neuron-specific Igfbp2 deficiency in the PFC induces cognitive dysfunction (A) Schematic of the experimental design. (B) Diagram of viral injection into the PFC (top) and representative image of viral expression (bottom); scale bars, 500 μm. (C) Representative western blot bands (top) and quantification of Igfbp2 protein levels in the PFC (bottom); n = 4 mice per group. (D) Schematic of the novel object recognition test, depicting the training phase (top) and the test phase (bottom). (E) Representative trajectory plots from the novel object recognition test. (F) Quantification of time spent investigating the novel object during the test phase; n = 8 mice per group. (G) Quantification of the number of investigations of the novel object during the test phase; n = 8 mice per group. (H) Schematic of the Y-maze test, depicting the training phase (top) and the test phase (bottom). (I) Representative trajectory plots from the Y-maze test. (J) Quantification of time spent in the novel arm during the test phase; n = 8 mice per group. (K) Quantification of the number of entries into the novel arm during the test phase; n = 8 mice per group. Analyzed by unpaired t test; ∗∗ p < 0.01. Data are presented as means ± SEM.

Journal: iScience

Article Title: Neuronal Igfbp2 deficiency in the prefrontal cortex impairs cognition through synaptic dysfunction in male mice

doi: 10.1016/j.isci.2026.115629

Figure Lengend Snippet: Neuron-specific Igfbp2 deficiency in the PFC induces cognitive dysfunction (A) Schematic of the experimental design. (B) Diagram of viral injection into the PFC (top) and representative image of viral expression (bottom); scale bars, 500 μm. (C) Representative western blot bands (top) and quantification of Igfbp2 protein levels in the PFC (bottom); n = 4 mice per group. (D) Schematic of the novel object recognition test, depicting the training phase (top) and the test phase (bottom). (E) Representative trajectory plots from the novel object recognition test. (F) Quantification of time spent investigating the novel object during the test phase; n = 8 mice per group. (G) Quantification of the number of investigations of the novel object during the test phase; n = 8 mice per group. (H) Schematic of the Y-maze test, depicting the training phase (top) and the test phase (bottom). (I) Representative trajectory plots from the Y-maze test. (J) Quantification of time spent in the novel arm during the test phase; n = 8 mice per group. (K) Quantification of the number of entries into the novel arm during the test phase; n = 8 mice per group. Analyzed by unpaired t test; ∗∗ p < 0.01. Data are presented as means ± SEM.

Article Snippet: Recombinant Igfbp2 protein (MCE; Cat# HY- P74846 ) was dissolved in sterile saline at 10 μg/μL.

Techniques: Injection, Expressing, Western Blot

Neuron-specific Igfbp2 deficiency in the PFC reduces excitatory synaptic transmission and neuronal excitability (A) Representative traces of sEPSC recorded from PFC neurons in AAV-scramble (top) and AAV-shRNA (bottom) groups. (B) Cumulative probability plots (main panel) and quantification (insert panel) of sEPSC frequency in AAV-Scramble and AAV-shRNA groups. (C) Cumulative probability plots (main panel) and quantification (insert panel) of sEPSC amplitude in AAV-Scramble and AAV-shRNA groups. (D) Representative traces of sIPSC recorded from PFC neurons in AAV-Scramble (top) and AAV-shRNA (bottom) groups. (E) Cumulative probability plots (main panel) and quantification (insert panel) of sIPSC frequency in AAV-Scramble and AAV-shRNA groups. (F) Cumulative probability plots (main panel) and quantification (insert panel) of sIPSC amplitude in AAV-Scramble and AAV-shRNA groups. (G) Representative traces of AP elicited by 200 pA current injections in PFC neurons from AAV-Scramble (left) and AAV-shRNA (right) groups. (H) Quantification of AP firing frequency in response to a range of current injections in PFC neurons from AAV-Scramble and AAV-shRNA groups. Analyzed by unpaired t test in B, C, E, and F, and two-way repeated-measure ANOVA in H; n = 8 neurons from 4 mice per group; ns: not significant, ∗∗ p < 0.01. Data are presented as means ± SEM.

Journal: iScience

Article Title: Neuronal Igfbp2 deficiency in the prefrontal cortex impairs cognition through synaptic dysfunction in male mice

doi: 10.1016/j.isci.2026.115629

Figure Lengend Snippet: Neuron-specific Igfbp2 deficiency in the PFC reduces excitatory synaptic transmission and neuronal excitability (A) Representative traces of sEPSC recorded from PFC neurons in AAV-scramble (top) and AAV-shRNA (bottom) groups. (B) Cumulative probability plots (main panel) and quantification (insert panel) of sEPSC frequency in AAV-Scramble and AAV-shRNA groups. (C) Cumulative probability plots (main panel) and quantification (insert panel) of sEPSC amplitude in AAV-Scramble and AAV-shRNA groups. (D) Representative traces of sIPSC recorded from PFC neurons in AAV-Scramble (top) and AAV-shRNA (bottom) groups. (E) Cumulative probability plots (main panel) and quantification (insert panel) of sIPSC frequency in AAV-Scramble and AAV-shRNA groups. (F) Cumulative probability plots (main panel) and quantification (insert panel) of sIPSC amplitude in AAV-Scramble and AAV-shRNA groups. (G) Representative traces of AP elicited by 200 pA current injections in PFC neurons from AAV-Scramble (left) and AAV-shRNA (right) groups. (H) Quantification of AP firing frequency in response to a range of current injections in PFC neurons from AAV-Scramble and AAV-shRNA groups. Analyzed by unpaired t test in B, C, E, and F, and two-way repeated-measure ANOVA in H; n = 8 neurons from 4 mice per group; ns: not significant, ∗∗ p < 0.01. Data are presented as means ± SEM.

Article Snippet: Recombinant Igfbp2 protein (MCE; Cat# HY- P74846 ) was dissolved in sterile saline at 10 μg/μL.

Techniques: Transmission Assay, shRNA

Neuron-specific Igfbp2 deficiency in the PFC disrupts synaptic integrity (A) Representative images of dendritic spines in the PFC from AAV-Scramble (left) and AAV-shRNA (right) groups; scale bars, 10 μm. (B) Quantification of dendritic spine density (number per 10 μm) in the PFC from AAV-Scramble and AAV-shRNA groups; n = 9 brain sections from 3 mice per group. (C) Representative western blot bands (top) and quantification of synapsin-1 protein levels (bottom) in the PFC from AAV-scramble and AAV-shRNA groups; n = 4 mice per group. (D) Representative western blot bands (top) and quantification of PSD-95 protein levels (bottom) in the PFC from AAV-Scramble and AAV-shRNA groups; n = 4 mice per group. Analyzed by unpaired t test; ∗ p < 0.05 and ∗∗∗ p < 0.001. Data are presented as means ± SEM.

Journal: iScience

Article Title: Neuronal Igfbp2 deficiency in the prefrontal cortex impairs cognition through synaptic dysfunction in male mice

doi: 10.1016/j.isci.2026.115629

Figure Lengend Snippet: Neuron-specific Igfbp2 deficiency in the PFC disrupts synaptic integrity (A) Representative images of dendritic spines in the PFC from AAV-Scramble (left) and AAV-shRNA (right) groups; scale bars, 10 μm. (B) Quantification of dendritic spine density (number per 10 μm) in the PFC from AAV-Scramble and AAV-shRNA groups; n = 9 brain sections from 3 mice per group. (C) Representative western blot bands (top) and quantification of synapsin-1 protein levels (bottom) in the PFC from AAV-scramble and AAV-shRNA groups; n = 4 mice per group. (D) Representative western blot bands (top) and quantification of PSD-95 protein levels (bottom) in the PFC from AAV-Scramble and AAV-shRNA groups; n = 4 mice per group. Analyzed by unpaired t test; ∗ p < 0.05 and ∗∗∗ p < 0.001. Data are presented as means ± SEM.

Article Snippet: Recombinant Igfbp2 protein (MCE; Cat# HY- P74846 ) was dissolved in sterile saline at 10 μg/μL.

Techniques: shRNA, Western Blot

Exogenous supplementation of Igfbp2 in the PFC rescues cognitive deficits induced by neuron-specific Igfbp2 deficiency (A) Schematic of the experimental design. (B) Diagram shows virus injection and cannula placement into the PFC (top), and a representative image of cannula position and viral expression in the PFC (bottom); scale bars, 500 μm. (C) Representative western blot bands (top) and quantification of Igfbp2 protein levels in the PFC (bottom); n = 4 mice per group. (D) Schematic of the novel object recognition test, depicting the training phase (top) and the test phase (bottom). (E) Representative trajectory plots from the novel object recognition test. (F) Quantification of time spent investigating the novel object during the test phase; n = 8 mice per group. (G) Quantification of the number of investigations of the novel object during the test phase; n = 8 mice per group. (H) Schematic of the Y-maze test, depicting the training phase (top) and the test phase (bottom). (I) Representative trajectory plots from the Y-maze test. (J) Quantification of time spent in the novel arm during the test phase; n = 8 mice per group. (K) Quantification of the number of entries into the novel arm during the test phase; n = 8 mice per group. Analyzed by unpaired t test; ∗∗ p < 0.01. Data are presented as means ± SEM.

Journal: iScience

Article Title: Neuronal Igfbp2 deficiency in the prefrontal cortex impairs cognition through synaptic dysfunction in male mice

doi: 10.1016/j.isci.2026.115629

Figure Lengend Snippet: Exogenous supplementation of Igfbp2 in the PFC rescues cognitive deficits induced by neuron-specific Igfbp2 deficiency (A) Schematic of the experimental design. (B) Diagram shows virus injection and cannula placement into the PFC (top), and a representative image of cannula position and viral expression in the PFC (bottom); scale bars, 500 μm. (C) Representative western blot bands (top) and quantification of Igfbp2 protein levels in the PFC (bottom); n = 4 mice per group. (D) Schematic of the novel object recognition test, depicting the training phase (top) and the test phase (bottom). (E) Representative trajectory plots from the novel object recognition test. (F) Quantification of time spent investigating the novel object during the test phase; n = 8 mice per group. (G) Quantification of the number of investigations of the novel object during the test phase; n = 8 mice per group. (H) Schematic of the Y-maze test, depicting the training phase (top) and the test phase (bottom). (I) Representative trajectory plots from the Y-maze test. (J) Quantification of time spent in the novel arm during the test phase; n = 8 mice per group. (K) Quantification of the number of entries into the novel arm during the test phase; n = 8 mice per group. Analyzed by unpaired t test; ∗∗ p < 0.01. Data are presented as means ± SEM.

Article Snippet: Recombinant Igfbp2 protein (MCE; Cat# HY- P74846 ) was dissolved in sterile saline at 10 μg/μL.

Techniques: Virus, Injection, Expressing, Western Blot

Exogenous supplementation of Igfbp2 in the PFC restores excitatory synaptic transmission and neuronal excitability impaired by neuron-specific Igfbp2 deficiency (A) Representative traces of sEPSC recorded from PFC neurons in saline (top) and Igfbp2 (bottom) groups. (B) Cumulative probability plots (main panel) and quantification (insert panel) of sEPSC frequency in saline (top) and Igfbp2 (bottom) groups. (C) Cumulative probability plots (main panel) and quantification (insert panel) of sEPSC amplitude in saline and Igfbp2 groups. (D) Representative traces of sIPSC recorded from PFC neurons in saline (top) and Igfbp2 (bottom) groups. (E) Cumulative probability plots (main panel) and quantification (insert panel) of sIPSC frequency in saline and Igfbp2 groups. (F) Cumulative probability plots (main panel) and quantification (insert panel) of sIPSC amplitude in saline and Igfbp2 groups. (G) Representative traces of AP elicited by 200 pA current injections in PFC neurons from saline (left) and Igfbp2 (right) groups. (H) Quantification of AP firing frequency in response to a range of current injections in PFC neurons from Saline (left) and Igfbp2 (right) groups. Analyzed by unpaired t test in B, C, E, and F, and two-way repeated-measure ANOVA in H; n = 8 neurons from 4 mice per group; ns: not significant, ∗∗ p < 0.01. Data are presented as means ± SEM.

Journal: iScience

Article Title: Neuronal Igfbp2 deficiency in the prefrontal cortex impairs cognition through synaptic dysfunction in male mice

doi: 10.1016/j.isci.2026.115629

Figure Lengend Snippet: Exogenous supplementation of Igfbp2 in the PFC restores excitatory synaptic transmission and neuronal excitability impaired by neuron-specific Igfbp2 deficiency (A) Representative traces of sEPSC recorded from PFC neurons in saline (top) and Igfbp2 (bottom) groups. (B) Cumulative probability plots (main panel) and quantification (insert panel) of sEPSC frequency in saline (top) and Igfbp2 (bottom) groups. (C) Cumulative probability plots (main panel) and quantification (insert panel) of sEPSC amplitude in saline and Igfbp2 groups. (D) Representative traces of sIPSC recorded from PFC neurons in saline (top) and Igfbp2 (bottom) groups. (E) Cumulative probability plots (main panel) and quantification (insert panel) of sIPSC frequency in saline and Igfbp2 groups. (F) Cumulative probability plots (main panel) and quantification (insert panel) of sIPSC amplitude in saline and Igfbp2 groups. (G) Representative traces of AP elicited by 200 pA current injections in PFC neurons from saline (left) and Igfbp2 (right) groups. (H) Quantification of AP firing frequency in response to a range of current injections in PFC neurons from Saline (left) and Igfbp2 (right) groups. Analyzed by unpaired t test in B, C, E, and F, and two-way repeated-measure ANOVA in H; n = 8 neurons from 4 mice per group; ns: not significant, ∗∗ p < 0.01. Data are presented as means ± SEM.

Article Snippet: Recombinant Igfbp2 protein (MCE; Cat# HY- P74846 ) was dissolved in sterile saline at 10 μg/μL.

Techniques: Transmission Assay, Saline

Exogenous supplementation of Igfbp2 in the PFC restores synaptic integrity disrupted by neuron-specific Igfbp2 deficiency (A) Representative images of dendritic spines in the PFC from saline (left) and Igfbp2 (right) groups; scale bars, 10 μm. (B) Quantification of dendritic spine density (number per 10 μm) in the PFC from saline and Igfbp2 groups; n = 9 brain sections from 3 mice per group. (C) Representative western blot bands (top) and quantification of synapsin-1 protein levels (bottom) in the PFC from AAV-Scramble and AAV-shRNA groups; n = 4 mice per group. (D) Representative western blot bands (top) and quantification of PSD-95 protein levels (bottom) in the PFC from AAV-Scramble and AAV-shRNA groups; n = 4 mice per group. Analyzed by unpaired t test; ∗ p < 0.05 and ∗∗∗ p < 0.001. Data are presented as means ± SEM.

Journal: iScience

Article Title: Neuronal Igfbp2 deficiency in the prefrontal cortex impairs cognition through synaptic dysfunction in male mice

doi: 10.1016/j.isci.2026.115629

Figure Lengend Snippet: Exogenous supplementation of Igfbp2 in the PFC restores synaptic integrity disrupted by neuron-specific Igfbp2 deficiency (A) Representative images of dendritic spines in the PFC from saline (left) and Igfbp2 (right) groups; scale bars, 10 μm. (B) Quantification of dendritic spine density (number per 10 μm) in the PFC from saline and Igfbp2 groups; n = 9 brain sections from 3 mice per group. (C) Representative western blot bands (top) and quantification of synapsin-1 protein levels (bottom) in the PFC from AAV-Scramble and AAV-shRNA groups; n = 4 mice per group. (D) Representative western blot bands (top) and quantification of PSD-95 protein levels (bottom) in the PFC from AAV-Scramble and AAV-shRNA groups; n = 4 mice per group. Analyzed by unpaired t test; ∗ p < 0.05 and ∗∗∗ p < 0.001. Data are presented as means ± SEM.

Article Snippet: Recombinant Igfbp2 protein (MCE; Cat# HY- P74846 ) was dissolved in sterile saline at 10 μg/μL.

Techniques: Saline, Western Blot, shRNA

Schematic summary of this study Neuron-specific Igfbp2 deficiency in the PFC impairs cognitive function by disrupting synaptic integrity, excitatory transmission, and neuronal activity, whereas exogenous Igfbp2 supplementation mitigates cognitive deficits by restoring synaptic integrity, excitatory transmission, and neuronal activity. PFC prefrontal cortex, sEPSC spontaneous excitatory postsynaptic currents, Igfbp2 insulin-like growth factor-binding protein 2.

Journal: iScience

Article Title: Neuronal Igfbp2 deficiency in the prefrontal cortex impairs cognition through synaptic dysfunction in male mice

doi: 10.1016/j.isci.2026.115629

Figure Lengend Snippet: Schematic summary of this study Neuron-specific Igfbp2 deficiency in the PFC impairs cognitive function by disrupting synaptic integrity, excitatory transmission, and neuronal activity, whereas exogenous Igfbp2 supplementation mitigates cognitive deficits by restoring synaptic integrity, excitatory transmission, and neuronal activity. PFC prefrontal cortex, sEPSC spontaneous excitatory postsynaptic currents, Igfbp2 insulin-like growth factor-binding protein 2.

Article Snippet: Recombinant Igfbp2 protein (MCE; Cat# HY- P74846 ) was dissolved in sterile saline at 10 μg/μL.

Techniques: Transmission Assay, Activity Assay, Binding Assay

Agrimol B blocks autophagic flux in PDAC cells. (A, B) Western blot analysis of P62 and CTSD in PANC-1 and AsPC-1 cells treated with Agrimol B for 24 h. (C, E, F) Immunofluorescence analysis of RFP-GFP-LC3 after PANC-1 and AsPC-1 cells were transfected with RFP-GFP-LC3 for 48 h, followed by treatment with or without Agrimol B for another 24 h. Scale bars, 10 μm. (D, G-L) Immunofluorescence analysis of the colocalization of endogenous LC3 with LAMP2 after treatment with Agrimol B or rapamycin for 24 h in PANC-1 and AsPC-1 cells. Scale bars, 10 μm. (M-O) Immunofluorescence analysis of LC3 in PDAC cells treated with or without Agrimol B in the presence or absence of HCQ. Scale bars, 10 μm.

Journal: Precision Clinical Medicine

Article Title: Agrimol B inhibits pancreatic ductal adenocarcinoma by induction of lethal mitophagy through decreasing mitochondrial transcription termination factor 3

doi: 10.1093/pcmedi/pbag009

Figure Lengend Snippet: Agrimol B blocks autophagic flux in PDAC cells. (A, B) Western blot analysis of P62 and CTSD in PANC-1 and AsPC-1 cells treated with Agrimol B for 24 h. (C, E, F) Immunofluorescence analysis of RFP-GFP-LC3 after PANC-1 and AsPC-1 cells were transfected with RFP-GFP-LC3 for 48 h, followed by treatment with or without Agrimol B for another 24 h. Scale bars, 10 μm. (D, G-L) Immunofluorescence analysis of the colocalization of endogenous LC3 with LAMP2 after treatment with Agrimol B or rapamycin for 24 h in PANC-1 and AsPC-1 cells. Scale bars, 10 μm. (M-O) Immunofluorescence analysis of LC3 in PDAC cells treated with or without Agrimol B in the presence or absence of HCQ. Scale bars, 10 μm.

Article Snippet: An anti-microtubule-associated protein light chain 3 (LC3) antibody (NB100-2220) was purchased from Novus, while anti-MTERF3 (EM1701-29) and lysosomal associated membrane protein 2 (LAMP2) (M1603-5) antibodies were purchased from HuaBio.

Techniques: Western Blot, Immunofluorescence, Transfection

SC suppresses apoptosis in vivo . Ovarian Granulosa Cells intervene in multiple pathophysiological indicators. Examination of apoptosis in laying hens by TUNEL assay. (A-B) Results revealed that treatment with different doses of SC resulted in decreased apoptosis. (C-J) The protein and mRNA expression of Bax, Cyt c, Cleaved Caspase-3, and Bcl-2.

Journal: Poultry Science

Article Title: Dietary semen cuscuta improves laying performance by stabilizing mitochondria-associated membranes (MAMs) and inhibiting granulosa cell apoptosis in laying hens

doi: 10.1016/j.psj.2026.106749

Figure Lengend Snippet: SC suppresses apoptosis in vivo . Ovarian Granulosa Cells intervene in multiple pathophysiological indicators. Examination of apoptosis in laying hens by TUNEL assay. (A-B) Results revealed that treatment with different doses of SC resulted in decreased apoptosis. (C-J) The protein and mRNA expression of Bax, Cyt c, Cleaved Caspase-3, and Bcl-2.

Article Snippet: The membranes underwent blocking with 5% skimmed milk diluted in PBS, and afterwards incubated employing primary antibodies against β-actin (GB15001, Servicebio, Wuhan, China), IP3R (GB11742, Servicebio, Wuhan, China), GRP75 (GB11852, Servicebio, Wuhan, China), VDAC1 ( GB111939 , Servicebio, Wuhan, China), Bcl-2 (26593-1-AP, Proteintech, Wuhan, China), Bax (50599-2-Ig, Proteintech, Wuhan, China), Cyt c (WL02410, Wanleibio, Shenyang, China), Cleaved Caspase-3 (WL01992, Wanleibio, Shenyang, China), GPR41 ( OM184469 , Omnimabs, California, United States), GPR43 ( OM255320 , Omnimabs, California, United States), Occludin (WL01996, Wanleibio, Shenyang, China) and ZO-1(21773-1-AP, Proteintech, Wuhan, China) overnight at 4°C with gentle shaking.

Techniques: In Vivo, TUNEL Assay, Expressing