Review



rabbit c terminal trip8b  (Proteintech)


Bioz Verified Symbol Proteintech is a verified supplier  
  • Logo
  • About
  • News
  • Press Release
  • Team
  • Advisors
  • Partners
  • Contact
  • Bioz Stars
  • Bioz vStars
    • 93
      Buy from Supplier

    Structured Review

    Proteintech rabbit c terminal trip8b
    A Illustration depicting the acute corticosterone treatment in the dorsal hippocampus. B Representative dorsal hippocampal slices immunolabeled with antibody against <t>TRIP8b.</t> Rectangle boxes depict the region of the slice used for quantification of the optical density. The arrows indicate increased perisomatic TRIP8b protein expression. C Quantification of TRIP8b protein expression from the perisomatic region to the distal dendritic region of CA1 from the dorsal hippocampus. D Representative dorsal hippocampal slices immunolabeled with antibody against HCN1. Rectangle boxes depict the region of the slice used for quantification of the optical density. The arrows indicate increased perisomatic HCN1 protein expression. E Quantification of HCN1 protein expression from the perisomatic region to the distal dendritic region of CA1 from the dorsal hippocampus. F , G We performed cell-attached voltage-clamp recordings. F Representative maximal h current traces in response to a 500-ms hyperpolarizing voltage step (−140 mV). G I h was significantly elevated in the dorsal CA1 neurons from corticosterone treatment compared with those from the vehicle-treated group. Dexamethasone reduced R in at RMP ( H ) and at −65 mV ( J ) in dorsal CA1 neurons. Corticosterone-induced decrease in R in at RMP ( H ) and at −65 mV ( J ) was blocked by RU 486, KT5720, and ZD7288. Changes in R in at RMP ( I ) and at −65 mV ( K ) were blocked by RU 486, KT5720, and ZD7288. Data are expressed as mean ± SEM.
    Rabbit C Terminal Trip8b, supplied by Proteintech, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/rabbit c terminal trip8b/product/Proteintech
    Average 93 stars, based on 1 article reviews
    rabbit c terminal trip8b - by Bioz Stars, 2026-03
    93/100 stars

    Images

    1) Product Images from "Glucocorticoid-glucocorticoid receptor-HCN1 channels reduce neuronal excitability in dorsal hippocampal CA1 neurons"

    Article Title: Glucocorticoid-glucocorticoid receptor-HCN1 channels reduce neuronal excitability in dorsal hippocampal CA1 neurons

    Journal: Molecular Psychiatry

    doi: 10.1038/s41380-022-01682-9

    A Illustration depicting the acute corticosterone treatment in the dorsal hippocampus. B Representative dorsal hippocampal slices immunolabeled with antibody against TRIP8b. Rectangle boxes depict the region of the slice used for quantification of the optical density. The arrows indicate increased perisomatic TRIP8b protein expression. C Quantification of TRIP8b protein expression from the perisomatic region to the distal dendritic region of CA1 from the dorsal hippocampus. D Representative dorsal hippocampal slices immunolabeled with antibody against HCN1. Rectangle boxes depict the region of the slice used for quantification of the optical density. The arrows indicate increased perisomatic HCN1 protein expression. E Quantification of HCN1 protein expression from the perisomatic region to the distal dendritic region of CA1 from the dorsal hippocampus. F , G We performed cell-attached voltage-clamp recordings. F Representative maximal h current traces in response to a 500-ms hyperpolarizing voltage step (−140 mV). G I h was significantly elevated in the dorsal CA1 neurons from corticosterone treatment compared with those from the vehicle-treated group. Dexamethasone reduced R in at RMP ( H ) and at −65 mV ( J ) in dorsal CA1 neurons. Corticosterone-induced decrease in R in at RMP ( H ) and at −65 mV ( J ) was blocked by RU 486, KT5720, and ZD7288. Changes in R in at RMP ( I ) and at −65 mV ( K ) were blocked by RU 486, KT5720, and ZD7288. Data are expressed as mean ± SEM.
    Figure Legend Snippet: A Illustration depicting the acute corticosterone treatment in the dorsal hippocampus. B Representative dorsal hippocampal slices immunolabeled with antibody against TRIP8b. Rectangle boxes depict the region of the slice used for quantification of the optical density. The arrows indicate increased perisomatic TRIP8b protein expression. C Quantification of TRIP8b protein expression from the perisomatic region to the distal dendritic region of CA1 from the dorsal hippocampus. D Representative dorsal hippocampal slices immunolabeled with antibody against HCN1. Rectangle boxes depict the region of the slice used for quantification of the optical density. The arrows indicate increased perisomatic HCN1 protein expression. E Quantification of HCN1 protein expression from the perisomatic region to the distal dendritic region of CA1 from the dorsal hippocampus. F , G We performed cell-attached voltage-clamp recordings. F Representative maximal h current traces in response to a 500-ms hyperpolarizing voltage step (−140 mV). G I h was significantly elevated in the dorsal CA1 neurons from corticosterone treatment compared with those from the vehicle-treated group. Dexamethasone reduced R in at RMP ( H ) and at −65 mV ( J ) in dorsal CA1 neurons. Corticosterone-induced decrease in R in at RMP ( H ) and at −65 mV ( J ) was blocked by RU 486, KT5720, and ZD7288. Changes in R in at RMP ( I ) and at −65 mV ( K ) were blocked by RU 486, KT5720, and ZD7288. Data are expressed as mean ± SEM.

    Techniques Used: Immunolabeling, Expressing

    A Timeline of CSDS, behavioral tests, electrophysiology, and biochemical assay. B CSDS produced the susceptible and resilient phenotype during the social interaction test. After 1 month ( C ) or 3 months ( D ) of no CSDS, susceptible mice showed persistent social avoidance during the social interaction test. E , F We performed whole-cell current-clamp recordings. E Representative voltage responses with depolarizing current step (210 pA; 750 ms) at RMP in dorsal CA1 neurons. F Dorsal CA1 neurons of susceptible group had lower action potential firing than control group, whereas the resilient group had higher action potential firing. G , H We performed cell-attached voltage-clamp recordings. G Representative maximal h current traces in response to a 500-ms hyperpolarizing voltage step (−140 mV). H I h was significantly elevated in the dorsal CA1 neurons from susceptible group compared with those from the control and resilient mice. Representative dorsal hippocampal slices immunolabeled with antibody against HCN1 ( I ) and TRIP8b ( K ). Rectangle boxes depict the region of the slice used for quantification of the optical density. The arrows indicate increased perisomatic HCN1 and TRIP8b protein expression. Quantification of HCN1 ( J ) and TRIP8b ( L ) protein expression from the perisomatic region to the distal dendritic region of CA1 from the dorsal hippocampus. M , N We performed whole-cell current-clamp recordings. M Corticosterone reduced R in at RMP of the dorsal CA1 neurons in the control and resilient groups, but had no effect on R in in susceptible group. N Changes in R in at RMP were much lower in susceptible group compared to the control and resilient groups. Data are expressed as mean ± SEM.
    Figure Legend Snippet: A Timeline of CSDS, behavioral tests, electrophysiology, and biochemical assay. B CSDS produced the susceptible and resilient phenotype during the social interaction test. After 1 month ( C ) or 3 months ( D ) of no CSDS, susceptible mice showed persistent social avoidance during the social interaction test. E , F We performed whole-cell current-clamp recordings. E Representative voltage responses with depolarizing current step (210 pA; 750 ms) at RMP in dorsal CA1 neurons. F Dorsal CA1 neurons of susceptible group had lower action potential firing than control group, whereas the resilient group had higher action potential firing. G , H We performed cell-attached voltage-clamp recordings. G Representative maximal h current traces in response to a 500-ms hyperpolarizing voltage step (−140 mV). H I h was significantly elevated in the dorsal CA1 neurons from susceptible group compared with those from the control and resilient mice. Representative dorsal hippocampal slices immunolabeled with antibody against HCN1 ( I ) and TRIP8b ( K ). Rectangle boxes depict the region of the slice used for quantification of the optical density. The arrows indicate increased perisomatic HCN1 and TRIP8b protein expression. Quantification of HCN1 ( J ) and TRIP8b ( L ) protein expression from the perisomatic region to the distal dendritic region of CA1 from the dorsal hippocampus. M , N We performed whole-cell current-clamp recordings. M Corticosterone reduced R in at RMP of the dorsal CA1 neurons in the control and resilient groups, but had no effect on R in in susceptible group. N Changes in R in at RMP were much lower in susceptible group compared to the control and resilient groups. Data are expressed as mean ± SEM.

    Techniques Used: Produced, Control, Immunolabeling, Expressing



    Similar Products

    rabbit c terminal trip8b  (Proteintech)
    93
    Proteintech rabbit c terminal trip8b
    A Illustration depicting the acute corticosterone treatment in the dorsal hippocampus. B Representative dorsal hippocampal slices immunolabeled with antibody against <t>TRIP8b.</t> Rectangle boxes depict the region of the slice used for quantification of the optical density. The arrows indicate increased perisomatic TRIP8b protein expression. C Quantification of TRIP8b protein expression from the perisomatic region to the distal dendritic region of CA1 from the dorsal hippocampus. D Representative dorsal hippocampal slices immunolabeled with antibody against HCN1. Rectangle boxes depict the region of the slice used for quantification of the optical density. The arrows indicate increased perisomatic HCN1 protein expression. E Quantification of HCN1 protein expression from the perisomatic region to the distal dendritic region of CA1 from the dorsal hippocampus. F , G We performed cell-attached voltage-clamp recordings. F Representative maximal h current traces in response to a 500-ms hyperpolarizing voltage step (−140 mV). G I h was significantly elevated in the dorsal CA1 neurons from corticosterone treatment compared with those from the vehicle-treated group. Dexamethasone reduced R in at RMP ( H ) and at −65 mV ( J ) in dorsal CA1 neurons. Corticosterone-induced decrease in R in at RMP ( H ) and at −65 mV ( J ) was blocked by RU 486, KT5720, and ZD7288. Changes in R in at RMP ( I ) and at −65 mV ( K ) were blocked by RU 486, KT5720, and ZD7288. Data are expressed as mean ± SEM.
    Rabbit C Terminal Trip8b, supplied by Proteintech, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/rabbit c terminal trip8b/product/Proteintech
    Average 93 stars, based on 1 article reviews
    rabbit c terminal trip8b - by Bioz Stars, 2026-03
    93/100 stars
    		  Buy from Supplier

    Image Search Results


    A Illustration depicting the acute corticosterone treatment in the dorsal hippocampus. B Representative dorsal hippocampal slices immunolabeled with antibody against TRIP8b. Rectangle boxes depict the region of the slice used for quantification of the optical density. The arrows indicate increased perisomatic TRIP8b protein expression. C Quantification of TRIP8b protein expression from the perisomatic region to the distal dendritic region of CA1 from the dorsal hippocampus. D Representative dorsal hippocampal slices immunolabeled with antibody against HCN1. Rectangle boxes depict the region of the slice used for quantification of the optical density. The arrows indicate increased perisomatic HCN1 protein expression. E Quantification of HCN1 protein expression from the perisomatic region to the distal dendritic region of CA1 from the dorsal hippocampus. F , G We performed cell-attached voltage-clamp recordings. F Representative maximal h current traces in response to a 500-ms hyperpolarizing voltage step (−140 mV). G I h was significantly elevated in the dorsal CA1 neurons from corticosterone treatment compared with those from the vehicle-treated group. Dexamethasone reduced R in at RMP ( H ) and at −65 mV ( J ) in dorsal CA1 neurons. Corticosterone-induced decrease in R in at RMP ( H ) and at −65 mV ( J ) was blocked by RU 486, KT5720, and ZD7288. Changes in R in at RMP ( I ) and at −65 mV ( K ) were blocked by RU 486, KT5720, and ZD7288. Data are expressed as mean ± SEM.

    Journal: Molecular Psychiatry

    Article Title: Glucocorticoid-glucocorticoid receptor-HCN1 channels reduce neuronal excitability in dorsal hippocampal CA1 neurons

    doi: 10.1038/s41380-022-01682-9

    Figure Lengend Snippet: A Illustration depicting the acute corticosterone treatment in the dorsal hippocampus. B Representative dorsal hippocampal slices immunolabeled with antibody against TRIP8b. Rectangle boxes depict the region of the slice used for quantification of the optical density. The arrows indicate increased perisomatic TRIP8b protein expression. C Quantification of TRIP8b protein expression from the perisomatic region to the distal dendritic region of CA1 from the dorsal hippocampus. D Representative dorsal hippocampal slices immunolabeled with antibody against HCN1. Rectangle boxes depict the region of the slice used for quantification of the optical density. The arrows indicate increased perisomatic HCN1 protein expression. E Quantification of HCN1 protein expression from the perisomatic region to the distal dendritic region of CA1 from the dorsal hippocampus. F , G We performed cell-attached voltage-clamp recordings. F Representative maximal h current traces in response to a 500-ms hyperpolarizing voltage step (−140 mV). G I h was significantly elevated in the dorsal CA1 neurons from corticosterone treatment compared with those from the vehicle-treated group. Dexamethasone reduced R in at RMP ( H ) and at −65 mV ( J ) in dorsal CA1 neurons. Corticosterone-induced decrease in R in at RMP ( H ) and at −65 mV ( J ) was blocked by RU 486, KT5720, and ZD7288. Changes in R in at RMP ( I ) and at −65 mV ( K ) were blocked by RU 486, KT5720, and ZD7288. Data are expressed as mean ± SEM.

    Article Snippet: Primary antibody in this study was used as follows; rabbit-anti-HCN1 (1:500, Invitrogen, Cat # PA5-78675), rabbit anti-HCN2 (1:500, Invitrogen, Cat # PA1-918), rabbit anti-HCN3 (1:500, Invitrogen, Cat # PA5-104434), rabbit anti-HCN4 (1:500, Invitrogen, Cat # PA5-111793), rabbit C-terminal TRIP8b (1:500, Proteintech, Cat #13084-1-AP), and rabbit anti-GR (1:500, Invitrogen, Cat # PA1-511A).

    Techniques: Immunolabeling, Expressing

    A Timeline of CSDS, behavioral tests, electrophysiology, and biochemical assay. B CSDS produced the susceptible and resilient phenotype during the social interaction test. After 1 month ( C ) or 3 months ( D ) of no CSDS, susceptible mice showed persistent social avoidance during the social interaction test. E , F We performed whole-cell current-clamp recordings. E Representative voltage responses with depolarizing current step (210 pA; 750 ms) at RMP in dorsal CA1 neurons. F Dorsal CA1 neurons of susceptible group had lower action potential firing than control group, whereas the resilient group had higher action potential firing. G , H We performed cell-attached voltage-clamp recordings. G Representative maximal h current traces in response to a 500-ms hyperpolarizing voltage step (−140 mV). H I h was significantly elevated in the dorsal CA1 neurons from susceptible group compared with those from the control and resilient mice. Representative dorsal hippocampal slices immunolabeled with antibody against HCN1 ( I ) and TRIP8b ( K ). Rectangle boxes depict the region of the slice used for quantification of the optical density. The arrows indicate increased perisomatic HCN1 and TRIP8b protein expression. Quantification of HCN1 ( J ) and TRIP8b ( L ) protein expression from the perisomatic region to the distal dendritic region of CA1 from the dorsal hippocampus. M , N We performed whole-cell current-clamp recordings. M Corticosterone reduced R in at RMP of the dorsal CA1 neurons in the control and resilient groups, but had no effect on R in in susceptible group. N Changes in R in at RMP were much lower in susceptible group compared to the control and resilient groups. Data are expressed as mean ± SEM.

    Journal: Molecular Psychiatry

    Article Title: Glucocorticoid-glucocorticoid receptor-HCN1 channels reduce neuronal excitability in dorsal hippocampal CA1 neurons

    doi: 10.1038/s41380-022-01682-9

    Figure Lengend Snippet: A Timeline of CSDS, behavioral tests, electrophysiology, and biochemical assay. B CSDS produced the susceptible and resilient phenotype during the social interaction test. After 1 month ( C ) or 3 months ( D ) of no CSDS, susceptible mice showed persistent social avoidance during the social interaction test. E , F We performed whole-cell current-clamp recordings. E Representative voltage responses with depolarizing current step (210 pA; 750 ms) at RMP in dorsal CA1 neurons. F Dorsal CA1 neurons of susceptible group had lower action potential firing than control group, whereas the resilient group had higher action potential firing. G , H We performed cell-attached voltage-clamp recordings. G Representative maximal h current traces in response to a 500-ms hyperpolarizing voltage step (−140 mV). H I h was significantly elevated in the dorsal CA1 neurons from susceptible group compared with those from the control and resilient mice. Representative dorsal hippocampal slices immunolabeled with antibody against HCN1 ( I ) and TRIP8b ( K ). Rectangle boxes depict the region of the slice used for quantification of the optical density. The arrows indicate increased perisomatic HCN1 and TRIP8b protein expression. Quantification of HCN1 ( J ) and TRIP8b ( L ) protein expression from the perisomatic region to the distal dendritic region of CA1 from the dorsal hippocampus. M , N We performed whole-cell current-clamp recordings. M Corticosterone reduced R in at RMP of the dorsal CA1 neurons in the control and resilient groups, but had no effect on R in in susceptible group. N Changes in R in at RMP were much lower in susceptible group compared to the control and resilient groups. Data are expressed as mean ± SEM.

    Article Snippet: Primary antibody in this study was used as follows; rabbit-anti-HCN1 (1:500, Invitrogen, Cat # PA5-78675), rabbit anti-HCN2 (1:500, Invitrogen, Cat # PA1-918), rabbit anti-HCN3 (1:500, Invitrogen, Cat # PA5-104434), rabbit anti-HCN4 (1:500, Invitrogen, Cat # PA5-111793), rabbit C-terminal TRIP8b (1:500, Proteintech, Cat #13084-1-AP), and rabbit anti-GR (1:500, Invitrogen, Cat # PA1-511A).

    Techniques: Produced, Control, Immunolabeling, Expressing