k252a  (Alomone Labs)


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    Structured Review

    Alomone Labs k252a
    <t>K252a</t> blocked the enhancing effects of Rh2 on neurogenesis. Compared to the (chronic unpredictable mild stress [CUMS] + Rh2)‐treated group, the increase of DCX + neurons in the DG of mice exposed to CUMS were significantly blocked by K252a. Scale bar: 100 μm. The results of analysis are expressed as the means ± SEM, n = 5. ** p
    K252a, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 94/100, based on 39 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/k252a/product/Alomone Labs
    Average 94 stars, based on 39 article reviews
    Price from $9.99 to $1999.99
    k252a - by Bioz Stars, 2022-12
    94/100 stars

    Images

    1) Product Images from "Ginsenoside Rh2 administration produces crucial antidepressant‐like effects in a CUMS‐induced mice model of depression). Ginsenoside Rh2 administration produces crucial antidepressant‐like effects in a CUMS‐induced mice model of depression"

    Article Title: Ginsenoside Rh2 administration produces crucial antidepressant‐like effects in a CUMS‐induced mice model of depression). Ginsenoside Rh2 administration produces crucial antidepressant‐like effects in a CUMS‐induced mice model of depression

    Journal: Brain and Behavior

    doi: 10.1002/brb3.2705

    K252a blocked the enhancing effects of Rh2 on neurogenesis. Compared to the (chronic unpredictable mild stress [CUMS] + Rh2)‐treated group, the increase of DCX + neurons in the DG of mice exposed to CUMS were significantly blocked by K252a. Scale bar: 100 μm. The results of analysis are expressed as the means ± SEM, n = 5. ** p
    Figure Legend Snippet: K252a blocked the enhancing effects of Rh2 on neurogenesis. Compared to the (chronic unpredictable mild stress [CUMS] + Rh2)‐treated group, the increase of DCX + neurons in the DG of mice exposed to CUMS were significantly blocked by K252a. Scale bar: 100 μm. The results of analysis are expressed as the means ± SEM, n = 5. ** p

    Techniques Used: Mouse Assay

    K252a decreased the antidepressant action of Rh2 in chronic unpredictable mild stress (CUMS)‐stressed mice. Co‐treatment with (K252a + Rh2) of the mice against CUMS showed the longer immobility time than the (CUMS + Rh2)‐treated mice in the forced swim test (FST)(a) and tail suspension test (TST) (b). K252a blocked the reversing effects of Rh2 on sucrose consumption of the CUMS‐treated mice (c). All data are expressed as the means ± SEM, n = 10. ** p
    Figure Legend Snippet: K252a decreased the antidepressant action of Rh2 in chronic unpredictable mild stress (CUMS)‐stressed mice. Co‐treatment with (K252a + Rh2) of the mice against CUMS showed the longer immobility time than the (CUMS + Rh2)‐treated mice in the forced swim test (FST)(a) and tail suspension test (TST) (b). K252a blocked the reversing effects of Rh2 on sucrose consumption of the CUMS‐treated mice (c). All data are expressed as the means ± SEM, n = 10. ** p

    Techniques Used: Mouse Assay

    The enhancing influence of Rh2 on the expression of BDNF‐CREB signaling pathway was blocked by the inhibitor K252a in mice exposed to chronic unpredictable mild stress (CUMS). BDNF, pERK/ERK, pAKT/AKT, and pCREB/CREB protein levels were lower in (CUMS + Rh2 + K252a)‐treated mice than the (CUMS + Rh2)‐treated mice. The obtained data are expressed as the means ± SEM, n = 5. ** p
    Figure Legend Snippet: The enhancing influence of Rh2 on the expression of BDNF‐CREB signaling pathway was blocked by the inhibitor K252a in mice exposed to chronic unpredictable mild stress (CUMS). BDNF, pERK/ERK, pAKT/AKT, and pCREB/CREB protein levels were lower in (CUMS + Rh2 + K252a)‐treated mice than the (CUMS + Rh2)‐treated mice. The obtained data are expressed as the means ± SEM, n = 5. ** p

    Techniques Used: Expressing, Mouse Assay

    2) Product Images from "Catalpol Enhances Neurogenesis And Inhibits Apoptosis Of New Neurons Via BDNF, But Not The BDNF/Trkb Pathway"

    Article Title: Catalpol Enhances Neurogenesis And Inhibits Apoptosis Of New Neurons Via BDNF, But Not The BDNF/Trkb Pathway

    Journal: Drug Design, Development and Therapy

    doi: 10.2147/DDDT.S223322

    Catalpol promoted neuronal survival, as evidenced by Nissl staining. Nissl staining showed more neuronal damage in the ipsilateral ischemic cortex, whereas catalpol, and K252a with catalpol, improved neuronal damage 7 days after stroke (400×, bar = 50 μm). ( A ) Control; ( B ) Model; ( C ) K252a; ( D ) K252a + 5 mg/kg catalpol; ( E ) 5 mg/kg catalpol; ( F )10 mg/kg catalpol; ( G ) Optical density of each group. *p
    Figure Legend Snippet: Catalpol promoted neuronal survival, as evidenced by Nissl staining. Nissl staining showed more neuronal damage in the ipsilateral ischemic cortex, whereas catalpol, and K252a with catalpol, improved neuronal damage 7 days after stroke (400×, bar = 50 μm). ( A ) Control; ( B ) Model; ( C ) K252a; ( D ) K252a + 5 mg/kg catalpol; ( E ) 5 mg/kg catalpol; ( F )10 mg/kg catalpol; ( G ) Optical density of each group. *p

    Techniques Used: Staining

    3) Product Images from "Neurotensin receptor type 2 protects B-cell chronic lymphocytic leukemia cells from apoptosis"

    Article Title: Neurotensin receptor type 2 protects B-cell chronic lymphocytic leukemia cells from apoptosis

    Journal: Oncogene

    doi: 10.1038/onc.2017.365

    NTSR2 phosphorylation in B-CLL and recruitment of G i α proteins. ( a ) Representative western blot analysis of Src phosphorylation in MEC-1 cells overexpressing NTSR2 (pCMV6-NTSR2) in the presence or absence of BDNF (100 ng/ml), pertussis toxin (PTX, 200 ng/ml) or K252a (100 nM) for 24 h. ( b ) Ratio of phosphorylated Src vs pan-Src protein, normalized against actin. Values are means±s.e.m. of three independent experiments in a.u. ( c , d ). After immunoprecipitation (IP) of NTSR2 from MEC-1 cells overexpressing NTSR2 (pCMV6-NTSR2) or not (EV), or from B-CLL cells in the presence or absence of BDNF (100 ng/ml) or NTS (40 μ M /ml), the immunocomplexes were immunoblotted (IB) with anti-G i α1/2 antibodies. ( e , f ) After immunoprecipitation (IP) of anti-pan-phosphoprotein was performed on MEC-1 cells overexpressing NTSR2 and B-CLL cells in the presence or absence of BDNF (100 ng/ml) or SR142948A (67 μ M ), the phosphorylation of NTSR2 was detected by immunoblotting (IB) with anti-NTSR2 antibodies. ( g ) Apoptotic ratio, assessed by cell death ELISA, in B-CLL in the presence or absence of SR142948A (67 μ M ) for 24 h. Values are mean ratios of apoptotic cells (±s.e.m.) of three independent experiments from different patients ( n =3). Significant P -values are indicated in the graphs * P
    Figure Legend Snippet: NTSR2 phosphorylation in B-CLL and recruitment of G i α proteins. ( a ) Representative western blot analysis of Src phosphorylation in MEC-1 cells overexpressing NTSR2 (pCMV6-NTSR2) in the presence or absence of BDNF (100 ng/ml), pertussis toxin (PTX, 200 ng/ml) or K252a (100 nM) for 24 h. ( b ) Ratio of phosphorylated Src vs pan-Src protein, normalized against actin. Values are means±s.e.m. of three independent experiments in a.u. ( c , d ). After immunoprecipitation (IP) of NTSR2 from MEC-1 cells overexpressing NTSR2 (pCMV6-NTSR2) or not (EV), or from B-CLL cells in the presence or absence of BDNF (100 ng/ml) or NTS (40 μ M /ml), the immunocomplexes were immunoblotted (IB) with anti-G i α1/2 antibodies. ( e , f ) After immunoprecipitation (IP) of anti-pan-phosphoprotein was performed on MEC-1 cells overexpressing NTSR2 and B-CLL cells in the presence or absence of BDNF (100 ng/ml) or SR142948A (67 μ M ), the phosphorylation of NTSR2 was detected by immunoblotting (IB) with anti-NTSR2 antibodies. ( g ) Apoptotic ratio, assessed by cell death ELISA, in B-CLL in the presence or absence of SR142948A (67 μ M ) for 24 h. Values are mean ratios of apoptotic cells (±s.e.m.) of three independent experiments from different patients ( n =3). Significant P -values are indicated in the graphs * P

    Techniques Used: Western Blot, Immunoprecipitation, Enzyme-linked Immunosorbent Assay

    4) Product Images from "Dual inhibition of BDNF/TrkB and autophagy: a promising therapeutic approach for colorectal cancer"

    Article Title: Dual inhibition of BDNF/TrkB and autophagy: a promising therapeutic approach for colorectal cancer

    Journal: Journal of Cellular and Molecular Medicine

    doi: 10.1111/jcmm.13181

    Effects of NT inhibitor (K252a), autophagy inhibitor (CQ) and dual treatment on tumoural growth. Nude mice were subcutaneously engrafted with SW480 or SW620 (1.10 6 cells). When tumours reached a volume of 300 mm 3 , animals were divided into different groups and treated with K252a for 21 days or with CQ for 12 days or with both molecules (see Materials and methods ). ( A ) Tumour growth was determined weekly. Results are expressed in mean tumour volumes (mm 3 ) ± S.D. in comparison with the non treated group (* P
    Figure Legend Snippet: Effects of NT inhibitor (K252a), autophagy inhibitor (CQ) and dual treatment on tumoural growth. Nude mice were subcutaneously engrafted with SW480 or SW620 (1.10 6 cells). When tumours reached a volume of 300 mm 3 , animals were divided into different groups and treated with K252a for 21 days or with CQ for 12 days or with both molecules (see Materials and methods ). ( A ) Tumour growth was determined weekly. Results are expressed in mean tumour volumes (mm 3 ) ± S.D. in comparison with the non treated group (* P

    Techniques Used: Mouse Assay

    Effects of dual treatment (K252a + CQ) on cell proliferation, cell death and vasculogenesis in tumour tissue originating from mice SW480 and SW620 xenografts. After being engrafted subcutaneously by SW480 or SW620, mice were treated by K252a + CQ as described in Materials and methods section. Tumour sample were collected from five xenograft mice for both cell lines. ( A ) Proliferation was determined by Ki67 immunostaining. Magnification was ×100. ( B ) Necrosis was quantified using HES staining. Aeras of necrosis are delimited by N. Magnification was ×50. Results are representative of the ratio between necrosis area and total tumour area obtained with the Nanozoomer Digital Pathology 2.ORS (Hamamatsu) version 2.5.88 software. ( C ) Tumour sample were lysed and total protein were extracted. VEGF and cleaved caspase 3 were assessed by Western blotting. The density of each band was calculated with ImageJ software. Images show representative results performed for each condition, for both xenografts cell lines.
    Figure Legend Snippet: Effects of dual treatment (K252a + CQ) on cell proliferation, cell death and vasculogenesis in tumour tissue originating from mice SW480 and SW620 xenografts. After being engrafted subcutaneously by SW480 or SW620, mice were treated by K252a + CQ as described in Materials and methods section. Tumour sample were collected from five xenograft mice for both cell lines. ( A ) Proliferation was determined by Ki67 immunostaining. Magnification was ×100. ( B ) Necrosis was quantified using HES staining. Aeras of necrosis are delimited by N. Magnification was ×50. Results are representative of the ratio between necrosis area and total tumour area obtained with the Nanozoomer Digital Pathology 2.ORS (Hamamatsu) version 2.5.88 software. ( C ) Tumour sample were lysed and total protein were extracted. VEGF and cleaved caspase 3 were assessed by Western blotting. The density of each band was calculated with ImageJ software. Images show representative results performed for each condition, for both xenografts cell lines.

    Techniques Used: Mouse Assay, Immunostaining, Staining, Digital Pathology, Software, Western Blot

    Metabolic activity, cell death analysis and PARP cleavage in CRC cell lines after K252a, CQ and K252a + CQ treatments. SW480 and SW620 were treated with K252a, CQ or both molecules for 72 hrs (see Materials and methods ). ( A ) Metabolic activity was assessed through MTT testing. Histograms show the means ± S.E.M. of at least three independent experiments (* P
    Figure Legend Snippet: Metabolic activity, cell death analysis and PARP cleavage in CRC cell lines after K252a, CQ and K252a + CQ treatments. SW480 and SW620 were treated with K252a, CQ or both molecules for 72 hrs (see Materials and methods ). ( A ) Metabolic activity was assessed through MTT testing. Histograms show the means ± S.E.M. of at least three independent experiments (* P

    Techniques Used: Activity Assay, MTT Assay

    Effect of tyrosine kinase receptor inhibitor (K252a) on TrkB/BDNF expression and autophagy induction. SW480 and SW620 were treated with 100 nM of K252a for 3 hrs, recovered, washed and total RNA and proteins were extracted (see Materials and methods ). ( A ) BDNF, Full Length (FL) and Truncated (Tr) TrkB, transcripts expression was assessed by qPCR. Histograms are representative of three independent experiments. The fold expression was obtained by the comparative cycle threshold method using the GAPDH RNA expression level as internal control. ( B ) BDNF, FL TrkB, Tr TrkB, phospho‐TrkB (P TrkB), AKT, phospho‐AKT (P AKT), mTOR and phospho‐mTOR (P mTOR), proteins expression were assessed by Western blotting. The density of each band representative for protein expression was calculated with ImageJ software. Images show representative results of three experiments. Statistically results are explained in comparison with control cells, normalized at 1 (* P
    Figure Legend Snippet: Effect of tyrosine kinase receptor inhibitor (K252a) on TrkB/BDNF expression and autophagy induction. SW480 and SW620 were treated with 100 nM of K252a for 3 hrs, recovered, washed and total RNA and proteins were extracted (see Materials and methods ). ( A ) BDNF, Full Length (FL) and Truncated (Tr) TrkB, transcripts expression was assessed by qPCR. Histograms are representative of three independent experiments. The fold expression was obtained by the comparative cycle threshold method using the GAPDH RNA expression level as internal control. ( B ) BDNF, FL TrkB, Tr TrkB, phospho‐TrkB (P TrkB), AKT, phospho‐AKT (P AKT), mTOR and phospho‐mTOR (P mTOR), proteins expression were assessed by Western blotting. The density of each band representative for protein expression was calculated with ImageJ software. Images show representative results of three experiments. Statistically results are explained in comparison with control cells, normalized at 1 (* P

    Techniques Used: Expressing, Real-time Polymerase Chain Reaction, RNA Expression, Western Blot, Software

    5) Product Images from "Dual inhibition of BDNF/TrkB and autophagy: a promising therapeutic approach for colorectal cancer"

    Article Title: Dual inhibition of BDNF/TrkB and autophagy: a promising therapeutic approach for colorectal cancer

    Journal: Journal of Cellular and Molecular Medicine

    doi: 10.1111/jcmm.13181

    Effects of NT inhibitor (K252a), autophagy inhibitor (CQ) and dual treatment on tumoural growth. Nude mice were subcutaneously engrafted with SW480 or SW620 (1.10 6 cells). When tumours reached a volume of 300 mm 3 , animals were divided into different groups and treated with K252a for 21 days or with CQ for 12 days or with both molecules (see Materials and methods ). ( A ) Tumour growth was determined weekly. Results are expressed in mean tumour volumes (mm 3 ) ± S.D. in comparison with the non treated group (* P
    Figure Legend Snippet: Effects of NT inhibitor (K252a), autophagy inhibitor (CQ) and dual treatment on tumoural growth. Nude mice were subcutaneously engrafted with SW480 or SW620 (1.10 6 cells). When tumours reached a volume of 300 mm 3 , animals were divided into different groups and treated with K252a for 21 days or with CQ for 12 days or with both molecules (see Materials and methods ). ( A ) Tumour growth was determined weekly. Results are expressed in mean tumour volumes (mm 3 ) ± S.D. in comparison with the non treated group (* P

    Techniques Used: Mouse Assay

    Effects of dual treatment (K252a + CQ) on cell proliferation, cell death and vasculogenesis in tumour tissue originating from mice SW480 and SW620 xenografts. After being engrafted subcutaneously by SW480 or SW620, mice were treated by K252a + CQ as described in Materials and methods section. Tumour sample were collected from five xenograft mice for both cell lines. ( A ) Proliferation was determined by Ki67 immunostaining. Magnification was ×100. ( B ) Necrosis was quantified using HES staining. Aeras of necrosis are delimited by N. Magnification was ×50. Results are representative of the ratio between necrosis area and total tumour area obtained with the Nanozoomer Digital Pathology 2.ORS (Hamamatsu) version 2.5.88 software. ( C ) Tumour sample were lysed and total protein were extracted. VEGF and cleaved caspase 3 were assessed by Western blotting. The density of each band was calculated with ImageJ software. Images show representative results performed for each condition, for both xenografts cell lines.
    Figure Legend Snippet: Effects of dual treatment (K252a + CQ) on cell proliferation, cell death and vasculogenesis in tumour tissue originating from mice SW480 and SW620 xenografts. After being engrafted subcutaneously by SW480 or SW620, mice were treated by K252a + CQ as described in Materials and methods section. Tumour sample were collected from five xenograft mice for both cell lines. ( A ) Proliferation was determined by Ki67 immunostaining. Magnification was ×100. ( B ) Necrosis was quantified using HES staining. Aeras of necrosis are delimited by N. Magnification was ×50. Results are representative of the ratio between necrosis area and total tumour area obtained with the Nanozoomer Digital Pathology 2.ORS (Hamamatsu) version 2.5.88 software. ( C ) Tumour sample were lysed and total protein were extracted. VEGF and cleaved caspase 3 were assessed by Western blotting. The density of each band was calculated with ImageJ software. Images show representative results performed for each condition, for both xenografts cell lines.

    Techniques Used: Mouse Assay, Immunostaining, Staining, Digital Pathology, Software, Western Blot

    Metabolic activity, cell death analysis and PARP cleavage in CRC cell lines after K252a, CQ and K252a + CQ treatments. SW480 and SW620 were treated with K252a, CQ or both molecules for 72 hrs (see Materials and methods ). ( A ) Metabolic activity was assessed through MTT testing. Histograms show the means ± S.E.M. of at least three independent experiments (* P
    Figure Legend Snippet: Metabolic activity, cell death analysis and PARP cleavage in CRC cell lines after K252a, CQ and K252a + CQ treatments. SW480 and SW620 were treated with K252a, CQ or both molecules for 72 hrs (see Materials and methods ). ( A ) Metabolic activity was assessed through MTT testing. Histograms show the means ± S.E.M. of at least three independent experiments (* P

    Techniques Used: Activity Assay, MTT Assay

    Effect of tyrosine kinase receptor inhibitor (K252a) on TrkB/BDNF expression and autophagy induction. SW480 and SW620 were treated with 100 nM of K252a for 3 hrs, recovered, washed and total RNA and proteins were extracted (see Materials and methods ). ( A ) BDNF, Full Length (FL) and Truncated (Tr) TrkB, transcripts expression was assessed by qPCR. Histograms are representative of three independent experiments. The fold expression was obtained by the comparative cycle threshold method using the GAPDH RNA expression level as internal control. ( B ) BDNF, FL TrkB, Tr TrkB, phospho‐TrkB (P TrkB), AKT, phospho‐AKT (P AKT), mTOR and phospho‐mTOR (P mTOR), proteins expression were assessed by Western blotting. The density of each band representative for protein expression was calculated with ImageJ software. Images show representative results of three experiments. Statistically results are explained in comparison with control cells, normalized at 1 (* P
    Figure Legend Snippet: Effect of tyrosine kinase receptor inhibitor (K252a) on TrkB/BDNF expression and autophagy induction. SW480 and SW620 were treated with 100 nM of K252a for 3 hrs, recovered, washed and total RNA and proteins were extracted (see Materials and methods ). ( A ) BDNF, Full Length (FL) and Truncated (Tr) TrkB, transcripts expression was assessed by qPCR. Histograms are representative of three independent experiments. The fold expression was obtained by the comparative cycle threshold method using the GAPDH RNA expression level as internal control. ( B ) BDNF, FL TrkB, Tr TrkB, phospho‐TrkB (P TrkB), AKT, phospho‐AKT (P AKT), mTOR and phospho‐mTOR (P mTOR), proteins expression were assessed by Western blotting. The density of each band representative for protein expression was calculated with ImageJ software. Images show representative results of three experiments. Statistically results are explained in comparison with control cells, normalized at 1 (* P

    Techniques Used: Expressing, Real-time Polymerase Chain Reaction, RNA Expression, Western Blot, Software

    6) Product Images from "Dual inhibition of BDNF/TrkB and autophagy: a promising therapeutic approach for colorectal cancer"

    Article Title: Dual inhibition of BDNF/TrkB and autophagy: a promising therapeutic approach for colorectal cancer

    Journal: Journal of Cellular and Molecular Medicine

    doi: 10.1111/jcmm.13181

    Effects of NT inhibitor (K252a), autophagy inhibitor (CQ) and dual treatment on tumoural growth. Nude mice were subcutaneously engrafted with SW480 or SW620 (1.10 6 cells). When tumours reached a volume of 300 mm 3 , animals were divided into different groups and treated with K252a for 21 days or with CQ for 12 days or with both molecules (see Materials and methods ). ( A ) Tumour growth was determined weekly. Results are expressed in mean tumour volumes (mm 3 ) ± S.D. in comparison with the non treated group (* P
    Figure Legend Snippet: Effects of NT inhibitor (K252a), autophagy inhibitor (CQ) and dual treatment on tumoural growth. Nude mice were subcutaneously engrafted with SW480 or SW620 (1.10 6 cells). When tumours reached a volume of 300 mm 3 , animals were divided into different groups and treated with K252a for 21 days or with CQ for 12 days or with both molecules (see Materials and methods ). ( A ) Tumour growth was determined weekly. Results are expressed in mean tumour volumes (mm 3 ) ± S.D. in comparison with the non treated group (* P

    Techniques Used: Mouse Assay

    Effects of dual treatment (K252a + CQ) on cell proliferation, cell death and vasculogenesis in tumour tissue originating from mice SW480 and SW620 xenografts. After being engrafted subcutaneously by SW480 or SW620, mice were treated by K252a + CQ as described in Materials and methods section. Tumour sample were collected from five xenograft mice for both cell lines. ( A ) Proliferation was determined by Ki67 immunostaining. Magnification was ×100. ( B ) Necrosis was quantified using HES staining. Aeras of necrosis are delimited by N. Magnification was ×50. Results are representative of the ratio between necrosis area and total tumour area obtained with the Nanozoomer Digital Pathology 2.ORS (Hamamatsu) version 2.5.88 software. ( C ) Tumour sample were lysed and total protein were extracted. VEGF and cleaved caspase 3 were assessed by Western blotting. The density of each band was calculated with ImageJ software. Images show representative results performed for each condition, for both xenografts cell lines.
    Figure Legend Snippet: Effects of dual treatment (K252a + CQ) on cell proliferation, cell death and vasculogenesis in tumour tissue originating from mice SW480 and SW620 xenografts. After being engrafted subcutaneously by SW480 or SW620, mice were treated by K252a + CQ as described in Materials and methods section. Tumour sample were collected from five xenograft mice for both cell lines. ( A ) Proliferation was determined by Ki67 immunostaining. Magnification was ×100. ( B ) Necrosis was quantified using HES staining. Aeras of necrosis are delimited by N. Magnification was ×50. Results are representative of the ratio between necrosis area and total tumour area obtained with the Nanozoomer Digital Pathology 2.ORS (Hamamatsu) version 2.5.88 software. ( C ) Tumour sample were lysed and total protein were extracted. VEGF and cleaved caspase 3 were assessed by Western blotting. The density of each band was calculated with ImageJ software. Images show representative results performed for each condition, for both xenografts cell lines.

    Techniques Used: Mouse Assay, Immunostaining, Staining, Digital Pathology, Software, Western Blot

    Metabolic activity, cell death analysis and PARP cleavage in CRC cell lines after K252a, CQ and K252a + CQ treatments. SW480 and SW620 were treated with K252a, CQ or both molecules for 72 hrs (see Materials and methods ). ( A ) Metabolic activity was assessed through MTT testing. Histograms show the means ± S.E.M. of at least three independent experiments (* P
    Figure Legend Snippet: Metabolic activity, cell death analysis and PARP cleavage in CRC cell lines after K252a, CQ and K252a + CQ treatments. SW480 and SW620 were treated with K252a, CQ or both molecules for 72 hrs (see Materials and methods ). ( A ) Metabolic activity was assessed through MTT testing. Histograms show the means ± S.E.M. of at least three independent experiments (* P

    Techniques Used: Activity Assay, MTT Assay

    Effect of tyrosine kinase receptor inhibitor (K252a) on TrkB/BDNF expression and autophagy induction. SW480 and SW620 were treated with 100 nM of K252a for 3 hrs, recovered, washed and total RNA and proteins were extracted (see Materials and methods ). ( A ) BDNF, Full Length (FL) and Truncated (Tr) TrkB, transcripts expression was assessed by qPCR. Histograms are representative of three independent experiments. The fold expression was obtained by the comparative cycle threshold method using the GAPDH RNA expression level as internal control. ( B ) BDNF, FL TrkB, Tr TrkB, phospho‐TrkB (P TrkB), AKT, phospho‐AKT (P AKT), mTOR and phospho‐mTOR (P mTOR), proteins expression were assessed by Western blotting. The density of each band representative for protein expression was calculated with ImageJ software. Images show representative results of three experiments. Statistically results are explained in comparison with control cells, normalized at 1 (* P
    Figure Legend Snippet: Effect of tyrosine kinase receptor inhibitor (K252a) on TrkB/BDNF expression and autophagy induction. SW480 and SW620 were treated with 100 nM of K252a for 3 hrs, recovered, washed and total RNA and proteins were extracted (see Materials and methods ). ( A ) BDNF, Full Length (FL) and Truncated (Tr) TrkB, transcripts expression was assessed by qPCR. Histograms are representative of three independent experiments. The fold expression was obtained by the comparative cycle threshold method using the GAPDH RNA expression level as internal control. ( B ) BDNF, FL TrkB, Tr TrkB, phospho‐TrkB (P TrkB), AKT, phospho‐AKT (P AKT), mTOR and phospho‐mTOR (P mTOR), proteins expression were assessed by Western blotting. The density of each band representative for protein expression was calculated with ImageJ software. Images show representative results of three experiments. Statistically results are explained in comparison with control cells, normalized at 1 (* P

    Techniques Used: Expressing, Real-time Polymerase Chain Reaction, RNA Expression, Western Blot, Software

    7) Product Images from "Dual inhibition of BDNF/TrkB and autophagy: a promising therapeutic approach for colorectal cancer"

    Article Title: Dual inhibition of BDNF/TrkB and autophagy: a promising therapeutic approach for colorectal cancer

    Journal: Journal of Cellular and Molecular Medicine

    doi: 10.1111/jcmm.13181

    Effects of NT inhibitor (K252a), autophagy inhibitor (CQ) and dual treatment on tumoural growth. Nude mice were subcutaneously engrafted with SW480 or SW620 (1.10 6 cells). When tumours reached a volume of 300 mm 3 , animals were divided into different groups and treated with K252a for 21 days or with CQ for 12 days or with both molecules (see Materials and methods ). ( A ) Tumour growth was determined weekly. Results are expressed in mean tumour volumes (mm 3 ) ± S.D. in comparison with the non treated group (* P
    Figure Legend Snippet: Effects of NT inhibitor (K252a), autophagy inhibitor (CQ) and dual treatment on tumoural growth. Nude mice were subcutaneously engrafted with SW480 or SW620 (1.10 6 cells). When tumours reached a volume of 300 mm 3 , animals were divided into different groups and treated with K252a for 21 days or with CQ for 12 days or with both molecules (see Materials and methods ). ( A ) Tumour growth was determined weekly. Results are expressed in mean tumour volumes (mm 3 ) ± S.D. in comparison with the non treated group (* P

    Techniques Used: Mouse Assay

    Effects of dual treatment (K252a + CQ) on cell proliferation, cell death and vasculogenesis in tumour tissue originating from mice SW480 and SW620 xenografts. After being engrafted subcutaneously by SW480 or SW620, mice were treated by K252a + CQ as described in Materials and methods section. Tumour sample were collected from five xenograft mice for both cell lines. ( A ) Proliferation was determined by Ki67 immunostaining. Magnification was ×100. ( B ) Necrosis was quantified using HES staining. Aeras of necrosis are delimited by N. Magnification was ×50. Results are representative of the ratio between necrosis area and total tumour area obtained with the Nanozoomer Digital Pathology 2.ORS (Hamamatsu) version 2.5.88 software. ( C ) Tumour sample were lysed and total protein were extracted. VEGF and cleaved caspase 3 were assessed by Western blotting. The density of each band was calculated with ImageJ software. Images show representative results performed for each condition, for both xenografts cell lines.
    Figure Legend Snippet: Effects of dual treatment (K252a + CQ) on cell proliferation, cell death and vasculogenesis in tumour tissue originating from mice SW480 and SW620 xenografts. After being engrafted subcutaneously by SW480 or SW620, mice were treated by K252a + CQ as described in Materials and methods section. Tumour sample were collected from five xenograft mice for both cell lines. ( A ) Proliferation was determined by Ki67 immunostaining. Magnification was ×100. ( B ) Necrosis was quantified using HES staining. Aeras of necrosis are delimited by N. Magnification was ×50. Results are representative of the ratio between necrosis area and total tumour area obtained with the Nanozoomer Digital Pathology 2.ORS (Hamamatsu) version 2.5.88 software. ( C ) Tumour sample were lysed and total protein were extracted. VEGF and cleaved caspase 3 were assessed by Western blotting. The density of each band was calculated with ImageJ software. Images show representative results performed for each condition, for both xenografts cell lines.

    Techniques Used: Mouse Assay, Immunostaining, Staining, Digital Pathology, Software, Western Blot

    Metabolic activity, cell death analysis and PARP cleavage in CRC cell lines after K252a, CQ and K252a + CQ treatments. SW480 and SW620 were treated with K252a, CQ or both molecules for 72 hrs (see Materials and methods ). ( A ) Metabolic activity was assessed through MTT testing. Histograms show the means ± S.E.M. of at least three independent experiments (* P
    Figure Legend Snippet: Metabolic activity, cell death analysis and PARP cleavage in CRC cell lines after K252a, CQ and K252a + CQ treatments. SW480 and SW620 were treated with K252a, CQ or both molecules for 72 hrs (see Materials and methods ). ( A ) Metabolic activity was assessed through MTT testing. Histograms show the means ± S.E.M. of at least three independent experiments (* P

    Techniques Used: Activity Assay, MTT Assay

    Effect of tyrosine kinase receptor inhibitor (K252a) on TrkB/BDNF expression and autophagy induction. SW480 and SW620 were treated with 100 nM of K252a for 3 hrs, recovered, washed and total RNA and proteins were extracted (see Materials and methods ). ( A ) BDNF, Full Length (FL) and Truncated (Tr) TrkB, transcripts expression was assessed by qPCR. Histograms are representative of three independent experiments. The fold expression was obtained by the comparative cycle threshold method using the GAPDH RNA expression level as internal control. ( B ) BDNF, FL TrkB, Tr TrkB, phospho‐TrkB (P TrkB), AKT, phospho‐AKT (P AKT), mTOR and phospho‐mTOR (P mTOR), proteins expression were assessed by Western blotting. The density of each band representative for protein expression was calculated with ImageJ software. Images show representative results of three experiments. Statistically results are explained in comparison with control cells, normalized at 1 (* P
    Figure Legend Snippet: Effect of tyrosine kinase receptor inhibitor (K252a) on TrkB/BDNF expression and autophagy induction. SW480 and SW620 were treated with 100 nM of K252a for 3 hrs, recovered, washed and total RNA and proteins were extracted (see Materials and methods ). ( A ) BDNF, Full Length (FL) and Truncated (Tr) TrkB, transcripts expression was assessed by qPCR. Histograms are representative of three independent experiments. The fold expression was obtained by the comparative cycle threshold method using the GAPDH RNA expression level as internal control. ( B ) BDNF, FL TrkB, Tr TrkB, phospho‐TrkB (P TrkB), AKT, phospho‐AKT (P AKT), mTOR and phospho‐mTOR (P mTOR), proteins expression were assessed by Western blotting. The density of each band representative for protein expression was calculated with ImageJ software. Images show representative results of three experiments. Statistically results are explained in comparison with control cells, normalized at 1 (* P

    Techniques Used: Expressing, Real-time Polymerase Chain Reaction, RNA Expression, Western Blot, Software

    8) Product Images from "Dual inhibition of BDNF/TrkB and autophagy: a promising therapeutic approach for colorectal cancer"

    Article Title: Dual inhibition of BDNF/TrkB and autophagy: a promising therapeutic approach for colorectal cancer

    Journal: Journal of Cellular and Molecular Medicine

    doi: 10.1111/jcmm.13181

    Effects of NT inhibitor (K252a), autophagy inhibitor (CQ) and dual treatment on tumoural growth. Nude mice were subcutaneously engrafted with SW480 or SW620 (1.10 6 cells). When tumours reached a volume of 300 mm 3 , animals were divided into different groups and treated with K252a for 21 days or with CQ for 12 days or with both molecules (see Materials and methods ). ( A ) Tumour growth was determined weekly. Results are expressed in mean tumour volumes (mm 3 ) ± S.D. in comparison with the non treated group (* P
    Figure Legend Snippet: Effects of NT inhibitor (K252a), autophagy inhibitor (CQ) and dual treatment on tumoural growth. Nude mice were subcutaneously engrafted with SW480 or SW620 (1.10 6 cells). When tumours reached a volume of 300 mm 3 , animals were divided into different groups and treated with K252a for 21 days or with CQ for 12 days or with both molecules (see Materials and methods ). ( A ) Tumour growth was determined weekly. Results are expressed in mean tumour volumes (mm 3 ) ± S.D. in comparison with the non treated group (* P

    Techniques Used: Mouse Assay

    Effects of dual treatment (K252a + CQ) on cell proliferation, cell death and vasculogenesis in tumour tissue originating from mice SW480 and SW620 xenografts. After being engrafted subcutaneously by SW480 or SW620, mice were treated by K252a + CQ as described in Materials and methods section. Tumour sample were collected from five xenograft mice for both cell lines. ( A ) Proliferation was determined by Ki67 immunostaining. Magnification was ×100. ( B ) Necrosis was quantified using HES staining. Aeras of necrosis are delimited by N. Magnification was ×50. Results are representative of the ratio between necrosis area and total tumour area obtained with the Nanozoomer Digital Pathology 2.ORS (Hamamatsu) version 2.5.88 software. ( C ) Tumour sample were lysed and total protein were extracted. VEGF and cleaved caspase 3 were assessed by Western blotting. The density of each band was calculated with ImageJ software. Images show representative results performed for each condition, for both xenografts cell lines.
    Figure Legend Snippet: Effects of dual treatment (K252a + CQ) on cell proliferation, cell death and vasculogenesis in tumour tissue originating from mice SW480 and SW620 xenografts. After being engrafted subcutaneously by SW480 or SW620, mice were treated by K252a + CQ as described in Materials and methods section. Tumour sample were collected from five xenograft mice for both cell lines. ( A ) Proliferation was determined by Ki67 immunostaining. Magnification was ×100. ( B ) Necrosis was quantified using HES staining. Aeras of necrosis are delimited by N. Magnification was ×50. Results are representative of the ratio between necrosis area and total tumour area obtained with the Nanozoomer Digital Pathology 2.ORS (Hamamatsu) version 2.5.88 software. ( C ) Tumour sample were lysed and total protein were extracted. VEGF and cleaved caspase 3 were assessed by Western blotting. The density of each band was calculated with ImageJ software. Images show representative results performed for each condition, for both xenografts cell lines.

    Techniques Used: Mouse Assay, Immunostaining, Staining, Digital Pathology, Software, Western Blot

    Metabolic activity, cell death analysis and PARP cleavage in CRC cell lines after K252a, CQ and K252a + CQ treatments. SW480 and SW620 were treated with K252a, CQ or both molecules for 72 hrs (see Materials and methods ). ( A ) Metabolic activity was assessed through MTT testing. Histograms show the means ± S.E.M. of at least three independent experiments (* P
    Figure Legend Snippet: Metabolic activity, cell death analysis and PARP cleavage in CRC cell lines after K252a, CQ and K252a + CQ treatments. SW480 and SW620 were treated with K252a, CQ or both molecules for 72 hrs (see Materials and methods ). ( A ) Metabolic activity was assessed through MTT testing. Histograms show the means ± S.E.M. of at least three independent experiments (* P

    Techniques Used: Activity Assay, MTT Assay

    Effect of tyrosine kinase receptor inhibitor (K252a) on TrkB/BDNF expression and autophagy induction. SW480 and SW620 were treated with 100 nM of K252a for 3 hrs, recovered, washed and total RNA and proteins were extracted (see Materials and methods ). ( A ) BDNF, Full Length (FL) and Truncated (Tr) TrkB, transcripts expression was assessed by qPCR. Histograms are representative of three independent experiments. The fold expression was obtained by the comparative cycle threshold method using the GAPDH RNA expression level as internal control. ( B ) BDNF, FL TrkB, Tr TrkB, phospho‐TrkB (P TrkB), AKT, phospho‐AKT (P AKT), mTOR and phospho‐mTOR (P mTOR), proteins expression were assessed by Western blotting. The density of each band representative for protein expression was calculated with ImageJ software. Images show representative results of three experiments. Statistically results are explained in comparison with control cells, normalized at 1 (* P
    Figure Legend Snippet: Effect of tyrosine kinase receptor inhibitor (K252a) on TrkB/BDNF expression and autophagy induction. SW480 and SW620 were treated with 100 nM of K252a for 3 hrs, recovered, washed and total RNA and proteins were extracted (see Materials and methods ). ( A ) BDNF, Full Length (FL) and Truncated (Tr) TrkB, transcripts expression was assessed by qPCR. Histograms are representative of three independent experiments. The fold expression was obtained by the comparative cycle threshold method using the GAPDH RNA expression level as internal control. ( B ) BDNF, FL TrkB, Tr TrkB, phospho‐TrkB (P TrkB), AKT, phospho‐AKT (P AKT), mTOR and phospho‐mTOR (P mTOR), proteins expression were assessed by Western blotting. The density of each band representative for protein expression was calculated with ImageJ software. Images show representative results of three experiments. Statistically results are explained in comparison with control cells, normalized at 1 (* P

    Techniques Used: Expressing, Real-time Polymerase Chain Reaction, RNA Expression, Western Blot, Software

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    Alomone Labs k252a
    <t>K252a</t> blocked the enhancing effects of Rh2 on neurogenesis. Compared to the (chronic unpredictable mild stress [CUMS] + Rh2)‐treated group, the increase of DCX + neurons in the DG of mice exposed to CUMS were significantly blocked by K252a. Scale bar: 100 μm. The results of analysis are expressed as the means ± SEM, n = 5. ** p
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    K252a blocked the enhancing effects of Rh2 on neurogenesis. Compared to the (chronic unpredictable mild stress [CUMS] + Rh2)‐treated group, the increase of DCX + neurons in the DG of mice exposed to CUMS were significantly blocked by K252a. Scale bar: 100 μm. The results of analysis are expressed as the means ± SEM, n = 5. ** p

    Journal: Brain and Behavior

    Article Title: Ginsenoside Rh2 administration produces crucial antidepressant‐like effects in a CUMS‐induced mice model of depression). Ginsenoside Rh2 administration produces crucial antidepressant‐like effects in a CUMS‐induced mice model of depression

    doi: 10.1002/brb3.2705

    Figure Lengend Snippet: K252a blocked the enhancing effects of Rh2 on neurogenesis. Compared to the (chronic unpredictable mild stress [CUMS] + Rh2)‐treated group, the increase of DCX + neurons in the DG of mice exposed to CUMS were significantly blocked by K252a. Scale bar: 100 μm. The results of analysis are expressed as the means ± SEM, n = 5. ** p

    Article Snippet: K252a was obtained from Alomone Laboratories (Jerusalem, Israel).

    Techniques: Mouse Assay

    K252a decreased the antidepressant action of Rh2 in chronic unpredictable mild stress (CUMS)‐stressed mice. Co‐treatment with (K252a + Rh2) of the mice against CUMS showed the longer immobility time than the (CUMS + Rh2)‐treated mice in the forced swim test (FST)(a) and tail suspension test (TST) (b). K252a blocked the reversing effects of Rh2 on sucrose consumption of the CUMS‐treated mice (c). All data are expressed as the means ± SEM, n = 10. ** p

    Journal: Brain and Behavior

    Article Title: Ginsenoside Rh2 administration produces crucial antidepressant‐like effects in a CUMS‐induced mice model of depression). Ginsenoside Rh2 administration produces crucial antidepressant‐like effects in a CUMS‐induced mice model of depression

    doi: 10.1002/brb3.2705

    Figure Lengend Snippet: K252a decreased the antidepressant action of Rh2 in chronic unpredictable mild stress (CUMS)‐stressed mice. Co‐treatment with (K252a + Rh2) of the mice against CUMS showed the longer immobility time than the (CUMS + Rh2)‐treated mice in the forced swim test (FST)(a) and tail suspension test (TST) (b). K252a blocked the reversing effects of Rh2 on sucrose consumption of the CUMS‐treated mice (c). All data are expressed as the means ± SEM, n = 10. ** p

    Article Snippet: K252a was obtained from Alomone Laboratories (Jerusalem, Israel).

    Techniques: Mouse Assay

    The enhancing influence of Rh2 on the expression of BDNF‐CREB signaling pathway was blocked by the inhibitor K252a in mice exposed to chronic unpredictable mild stress (CUMS). BDNF, pERK/ERK, pAKT/AKT, and pCREB/CREB protein levels were lower in (CUMS + Rh2 + K252a)‐treated mice than the (CUMS + Rh2)‐treated mice. The obtained data are expressed as the means ± SEM, n = 5. ** p

    Journal: Brain and Behavior

    Article Title: Ginsenoside Rh2 administration produces crucial antidepressant‐like effects in a CUMS‐induced mice model of depression). Ginsenoside Rh2 administration produces crucial antidepressant‐like effects in a CUMS‐induced mice model of depression

    doi: 10.1002/brb3.2705

    Figure Lengend Snippet: The enhancing influence of Rh2 on the expression of BDNF‐CREB signaling pathway was blocked by the inhibitor K252a in mice exposed to chronic unpredictable mild stress (CUMS). BDNF, pERK/ERK, pAKT/AKT, and pCREB/CREB protein levels were lower in (CUMS + Rh2 + K252a)‐treated mice than the (CUMS + Rh2)‐treated mice. The obtained data are expressed as the means ± SEM, n = 5. ** p

    Article Snippet: K252a was obtained from Alomone Laboratories (Jerusalem, Israel).

    Techniques: Expressing, Mouse Assay

    LTD at MF synapses is not mediated via p75NTR or TrkB receptor signaling. ( a ), ( c ) and ( d ) MF LTD is not impaired in the presence of bath applied TAT-Pep5 (1 µM, a ), LM11A31 (100 nM, c ) or K252a (200 nM, d ) in comparison to the respective solvent controls (filled circle: BSA ( a , n = 8/N = 6), ACSF ( c , n = 16/N = 12) and DMSO ( d , n = 12/N = 6); filled gray circle: TAT-Pep5 ( a , n = 11/N = 10), LM11A31 ( c , n = 11/N = 6) and K252a ( d , n = 9/N = 5)). b) Recordings in slices of p75NTR EXIV−/− mice displayed no influence of p75NTR chronic deficiency on LTD magnitudes at MF synapses (filled circle: p75NTR wildtype (n = 8/N = 5); filled gray circle: p75NTR EXIV−/− (n = 12/N = 7)). ( e ) Unaltered MF LTD in the presence of bath applied ANA-12 (20 µM), in comparison to the respective solvent control (filled circle: DMSO (n = 16/N = 11); filled gray circle: ANA-12 ( e , n = 11/N = 6). The figure insets show representative averaged original fEPSP traces. For all MF-LTD experiments, “1” indicates mean fEPSP amplitudes of first 10 min of baseline and “2” depicts mean fEPSP amplitudes between 55 and 60 min after induction of LTD. Data expressed as mean ± SEM. Corresponding scale bars are shown as insets.

    Journal: Scientific Reports

    Article Title: Long-term depression at hippocampal mossy fiber-CA3 synapses involves BDNF but is not mediated by p75NTR signaling

    doi: 10.1038/s41598-021-87769-9

    Figure Lengend Snippet: LTD at MF synapses is not mediated via p75NTR or TrkB receptor signaling. ( a ), ( c ) and ( d ) MF LTD is not impaired in the presence of bath applied TAT-Pep5 (1 µM, a ), LM11A31 (100 nM, c ) or K252a (200 nM, d ) in comparison to the respective solvent controls (filled circle: BSA ( a , n = 8/N = 6), ACSF ( c , n = 16/N = 12) and DMSO ( d , n = 12/N = 6); filled gray circle: TAT-Pep5 ( a , n = 11/N = 10), LM11A31 ( c , n = 11/N = 6) and K252a ( d , n = 9/N = 5)). b) Recordings in slices of p75NTR EXIV−/− mice displayed no influence of p75NTR chronic deficiency on LTD magnitudes at MF synapses (filled circle: p75NTR wildtype (n = 8/N = 5); filled gray circle: p75NTR EXIV−/− (n = 12/N = 7)). ( e ) Unaltered MF LTD in the presence of bath applied ANA-12 (20 µM), in comparison to the respective solvent control (filled circle: DMSO (n = 16/N = 11); filled gray circle: ANA-12 ( e , n = 11/N = 6). The figure insets show representative averaged original fEPSP traces. For all MF-LTD experiments, “1” indicates mean fEPSP amplitudes of first 10 min of baseline and “2” depicts mean fEPSP amplitudes between 55 and 60 min after induction of LTD. Data expressed as mean ± SEM. Corresponding scale bars are shown as insets.

    Article Snippet: To test for acute effects of BDNF signaling via tropomyosin related kinase (Trk) B, the tyrosine kinase inhibitor K252a (200 nM, Alomone Labs; Israel; dissolved in 0.1% Dimethyl sulfoxide (DMSO; Sigma Aldrich, Germany) was bath applied.

    Techniques: Mouse Assay