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Effects of <t>exogenous</t> <t>IGF1</t> on cell viability and mitochondrial dysfunction in CIH-exposed HT22 cells. (A) Effects of various IGF1 concentrations on cell viability. (B) TEM was used to detect mitochondria in HT22 cells that had been exposed to CIH (20000 × ). (C and E) Effects of exogenous IGF1 on the mitochondrial membrane potential of HT22 cells (scale bar = 50 μm). (D and F) Effects of exogenous IGF1 on ROS production in the mitochondria of CIH-exposed HT22 cells (scale bar = 25 μm). (G) Effects of exogenous IGF1 on mitochondrial ATP levels in CIH-exposed HT22 cells. (H) Effects of exogenous IGF1 on the level of mitochondrial respiratory chain complex Ι in HT22 cells exposed to CIH. (I) BDNF expression in CIH-exposed HT22 cells. (J) PSD-95 expression in CIH-exposed HT22 cells. (K) P-CREB/CREB expression in HT22 cells exposed to CIH. (L) <t>P-ERK/ERK</t> expression in CIH-exposed HT22 cells. The results are presented as the mean ± standard deviation (SD). n = 3. ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001 versus the CON group, # P < 0.05, ## P < 0.01, ### P < 0.001 versus the CIH group.
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Effects of <t>exogenous</t> <t>IGF1</t> on cell viability and mitochondrial dysfunction in CIH-exposed HT22 cells. (A) Effects of various IGF1 concentrations on cell viability. (B) TEM was used to detect mitochondria in HT22 cells that had been exposed to CIH (20000 × ). (C and E) Effects of exogenous IGF1 on the mitochondrial membrane potential of HT22 cells (scale bar = 50 μm). (D and F) Effects of exogenous IGF1 on ROS production in the mitochondria of CIH-exposed HT22 cells (scale bar = 25 μm). (G) Effects of exogenous IGF1 on mitochondrial ATP levels in CIH-exposed HT22 cells. (H) Effects of exogenous IGF1 on the level of mitochondrial respiratory chain complex Ι in HT22 cells exposed to CIH. (I) BDNF expression in CIH-exposed HT22 cells. (J) PSD-95 expression in CIH-exposed HT22 cells. (K) P-CREB/CREB expression in HT22 cells exposed to CIH. (L) <t>P-ERK/ERK</t> expression in CIH-exposed HT22 cells. The results are presented as the mean ± standard deviation (SD). n = 3. ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001 versus the CON group, # P < 0.05, ## P < 0.01, ### P < 0.001 versus the CIH group.
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Effects of exogenous IGF1 on cell viability and mitochondrial dysfunction in CIH-exposed HT22 cells. (A) Effects of various IGF1 concentrations on cell viability. (B) TEM was used to detect mitochondria in HT22 cells that had been exposed to CIH (20000 × ). (C and E) Effects of exogenous IGF1 on the mitochondrial membrane potential of HT22 cells (scale bar = 50 μm). (D and F) Effects of exogenous IGF1 on ROS production in the mitochondria of CIH-exposed HT22 cells (scale bar = 25 μm). (G) Effects of exogenous IGF1 on mitochondrial ATP levels in CIH-exposed HT22 cells. (H) Effects of exogenous IGF1 on the level of mitochondrial respiratory chain complex Ι in HT22 cells exposed to CIH. (I) BDNF expression in CIH-exposed HT22 cells. (J) PSD-95 expression in CIH-exposed HT22 cells. (K) P-CREB/CREB expression in HT22 cells exposed to CIH. (L) P-ERK/ERK expression in CIH-exposed HT22 cells. The results are presented as the mean ± standard deviation (SD). n = 3. ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001 versus the CON group, # P < 0.05, ## P < 0.01, ### P < 0.001 versus the CIH group.

Journal: Journal of Traditional and Complementary Medicine

Article Title: Role of IGF1/IGFR signaling pathway in neuroprotective effect of Shengmai Dihuang Decoction on CIH-induced cognitive impairment

doi: 10.1016/j.jtcme.2024.11.014

Figure Lengend Snippet: Effects of exogenous IGF1 on cell viability and mitochondrial dysfunction in CIH-exposed HT22 cells. (A) Effects of various IGF1 concentrations on cell viability. (B) TEM was used to detect mitochondria in HT22 cells that had been exposed to CIH (20000 × ). (C and E) Effects of exogenous IGF1 on the mitochondrial membrane potential of HT22 cells (scale bar = 50 μm). (D and F) Effects of exogenous IGF1 on ROS production in the mitochondria of CIH-exposed HT22 cells (scale bar = 25 μm). (G) Effects of exogenous IGF1 on mitochondrial ATP levels in CIH-exposed HT22 cells. (H) Effects of exogenous IGF1 on the level of mitochondrial respiratory chain complex Ι in HT22 cells exposed to CIH. (I) BDNF expression in CIH-exposed HT22 cells. (J) PSD-95 expression in CIH-exposed HT22 cells. (K) P-CREB/CREB expression in HT22 cells exposed to CIH. (L) P-ERK/ERK expression in CIH-exposed HT22 cells. The results are presented as the mean ± standard deviation (SD). n = 3. ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001 versus the CON group, # P < 0.05, ## P < 0.01, ### P < 0.001 versus the CIH group.

Article Snippet: IGF1 (bs-0014R), IGFR (bs-4985R), P-CREB (bs-5256R), CREB (bsm-33196R), P-ERK (bs-3016R), and ERK (bsm-52259R) were purchased from Bioss Antibodies (Woburn, MA, USA).

Techniques: Membrane, Expressing, Standard Deviation

Effects of SDD on cell viability and mitochondrial dysfunction under CIH circumstances in HT22 cells. (A) TEM was used to detect mitochondria in CIH-exposed HT22 cells (20000 × ). (B and D) Impact of SDD on the potential of mitochondria in CIH-exposed HT22 cells (scale bar = 50 μm). (C and E) Effects of SDD on mitochondrial ROS in CIH-exposed HT22 cells (scale bar = 25 μm). (F) Effects of SDD on mitochondrial ATP levels in CIH-exposed HT22 cells. (G) Effects of SDD on the level of mitochondrial respiratory chain complex Ι in CIH-exposed HT22 cells. (H) Cell viability after CIH exposure. (I–J) PSD-95 and BDNF expression in CIH-exposed HT22 cells. (K–L) P-CREB/CREB and P-ERK/ERK expression in CIH-exposed HT22 cells. The results are presented as the mean ± standard deviation (SD). n = 3. ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001 versus the CON group, # P < 0.05, ## P < 0.01, ### P < 0.001 versus the CIH group.

Journal: Journal of Traditional and Complementary Medicine

Article Title: Role of IGF1/IGFR signaling pathway in neuroprotective effect of Shengmai Dihuang Decoction on CIH-induced cognitive impairment

doi: 10.1016/j.jtcme.2024.11.014

Figure Lengend Snippet: Effects of SDD on cell viability and mitochondrial dysfunction under CIH circumstances in HT22 cells. (A) TEM was used to detect mitochondria in CIH-exposed HT22 cells (20000 × ). (B and D) Impact of SDD on the potential of mitochondria in CIH-exposed HT22 cells (scale bar = 50 μm). (C and E) Effects of SDD on mitochondrial ROS in CIH-exposed HT22 cells (scale bar = 25 μm). (F) Effects of SDD on mitochondrial ATP levels in CIH-exposed HT22 cells. (G) Effects of SDD on the level of mitochondrial respiratory chain complex Ι in CIH-exposed HT22 cells. (H) Cell viability after CIH exposure. (I–J) PSD-95 and BDNF expression in CIH-exposed HT22 cells. (K–L) P-CREB/CREB and P-ERK/ERK expression in CIH-exposed HT22 cells. The results are presented as the mean ± standard deviation (SD). n = 3. ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001 versus the CON group, # P < 0.05, ## P < 0.01, ### P < 0.001 versus the CIH group.

Article Snippet: IGF1 (bs-0014R), IGFR (bs-4985R), P-CREB (bs-5256R), CREB (bsm-33196R), P-ERK (bs-3016R), and ERK (bsm-52259R) were purchased from Bioss Antibodies (Woburn, MA, USA).

Techniques: Expressing, Standard Deviation

Role of IGF1 siRNA and AG1024 in improving the effects of SDD on neuronal injury in CIH-exposed HT22 cells. (A–B) PSD-95 and BDNF expression in CIH-exposed HT22 cells. (C–D) P-CREB/CREB and P-ERK/ERK expression in CIH-exposed HT22 cells. (E) TEM was used to detect mitochondria in CIH-exposed HT22 cells (20000 × ). (F and H) Mitochondrial membrane potential in CIH-exposed HT22 cells (scale bar = 50 μm). (G and I) Mitochondrial ROS in CIH-exposed HT22 cells (scale bar = 25 μm). (J) Mitochondrial ATP levels in CIH-exposed HT22 cells. (K) The level of mitochondrial respiratory chain complex Ι in CIH-exposed HT22 cells. (L) The viability of CIH-exposed HT22 cells. The results are presented as the mean ± standard deviation (SD). n = 3. ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001 versus the CON group, # P < 0.05, ## P < 0.01 versus the CIH group, △ P < 0.05, △△ P < 0.01, △△△ P < 0.001 versus the SDD group.

Journal: Journal of Traditional and Complementary Medicine

Article Title: Role of IGF1/IGFR signaling pathway in neuroprotective effect of Shengmai Dihuang Decoction on CIH-induced cognitive impairment

doi: 10.1016/j.jtcme.2024.11.014

Figure Lengend Snippet: Role of IGF1 siRNA and AG1024 in improving the effects of SDD on neuronal injury in CIH-exposed HT22 cells. (A–B) PSD-95 and BDNF expression in CIH-exposed HT22 cells. (C–D) P-CREB/CREB and P-ERK/ERK expression in CIH-exposed HT22 cells. (E) TEM was used to detect mitochondria in CIH-exposed HT22 cells (20000 × ). (F and H) Mitochondrial membrane potential in CIH-exposed HT22 cells (scale bar = 50 μm). (G and I) Mitochondrial ROS in CIH-exposed HT22 cells (scale bar = 25 μm). (J) Mitochondrial ATP levels in CIH-exposed HT22 cells. (K) The level of mitochondrial respiratory chain complex Ι in CIH-exposed HT22 cells. (L) The viability of CIH-exposed HT22 cells. The results are presented as the mean ± standard deviation (SD). n = 3. ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001 versus the CON group, # P < 0.05, ## P < 0.01 versus the CIH group, △ P < 0.05, △△ P < 0.01, △△△ P < 0.001 versus the SDD group.

Article Snippet: IGF1 (bs-0014R), IGFR (bs-4985R), P-CREB (bs-5256R), CREB (bsm-33196R), P-ERK (bs-3016R), and ERK (bsm-52259R) were purchased from Bioss Antibodies (Woburn, MA, USA).

Techniques: Expressing, Membrane, Standard Deviation