Antibody data
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- Antigen structure
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- Product number
- 44-612G - Provider product page
- Provider
- Invitrogen Antibodies
- Product name
- Phospho-ERK5 (Thr218, Tyr220) Polyclonal Antibody
- Antibody type
- Polyclonal
- Antigen
- Synthetic peptide
- Reactivity
- Human
- Host
- Rabbit
- Isotype
- IgG
- Vial size
- 100 µL
- Storage
- -20°C
Submitted references Dexmedetomidine and Netrin-1 Combination Therapy Inhibits Endoplasmic Reticulum Stress by Regulating the ERK5/MEF2A Pathway to Attenuate Cerebral Ischemia Injury.
MAP kinase kinase kinase-2 (MEKK2) regulates hypertrophic remodeling of the right ventricle in hypoxia-induced pulmonary hypertension.
Abl-kinase-sensitive levels of ERK5 and its intrinsic basal activity contribute to leukaemia cell survival.
Phosphotyrosine-specific phosphatase PTP-SL regulates the ERK5 signaling pathway.
Yin JW, Li J, Ren YM, Li Y, Wang RX, Wang S, Zuo YX
Frontiers in neuroscience 2021;15:641345
Frontiers in neuroscience 2021;15:641345
MAP kinase kinase kinase-2 (MEKK2) regulates hypertrophic remodeling of the right ventricle in hypoxia-induced pulmonary hypertension.
Brown RD, Ambler SK, Li M, Sullivan TM, Henry LN, Crossno JT Jr, Long CS, Garrington TP, Stenmark KR
American journal of physiology. Heart and circulatory physiology 2013 Jan 15;304(2):H269-81
American journal of physiology. Heart and circulatory physiology 2013 Jan 15;304(2):H269-81
Abl-kinase-sensitive levels of ERK5 and its intrinsic basal activity contribute to leukaemia cell survival.
Buschbeck M, Hofbauer S, Di Croce L, Keri G, Ullrich A
EMBO reports 2005 Jan;6(1):63-9
EMBO reports 2005 Jan;6(1):63-9
Phosphotyrosine-specific phosphatase PTP-SL regulates the ERK5 signaling pathway.
Buschbeck M, Eickhoff J, Sommer MN, Ullrich A
The Journal of biological chemistry 2002 Aug 16;277(33):29503-9
The Journal of biological chemistry 2002 Aug 16;277(33):29503-9
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Supportive validation
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- Invitrogen Antibodies (provider)
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- Invitrogen Antibodies (provider)
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- Experimental details
- FIGURE 6 Dexmedetomidine and Netrin-1 up-regulated the expression of the ERK5 and MEF2A after MCAO injury and OGD injury. (A) MEF2A expressions in hippocampus after MCAO injury. Immunofluorescence staining exhibited positive cells of MEF2A. Green indicated MEF2A expression in plasm of pyramidal neurons, and blue indicated the nucleus. Scale bar = 100 mum. (B) p-ERK5 expressions in hippocampus after MCAO injury. Immunofluorescence staining exhibited positive cells of p-ERK5. Green indicated p-ERK5 expression in nucleus of pyramidal neurons, and red indicated the nucleus. Scale bar = 100 mum. (C,D) Western blot analysis of MEF2A, ERK5 and p-ERK5 proteins, beta-actin was used as an internal control. (E-I) Quantitative analysis of MEF2A and GRP78 expression levels. (F-J) Quantitative analysis of p-ERK5 expression levels. * P < 0.05, ** P < 0.01 and *** P < 0.001 using one-way ANOVA followed by Tukey's post hoc tests.
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- FIGURE 7 Knockdown MEF2A weakened the therapeutic effect of dexmedetomidine combined with Netrin-1 after MCAO and OGD injuries. (A,B) Immunofluorescence staining exhibited downregulation in MEF2A expression in the hippocampus at 14 days after AAV9-MEF2A RNAi microinjection. (C,D) Western blot analysis shows downregulation in MEF2A expression in the hippocampus at 14 days after AAV9-MEF2A RNAi microinjection. (E) The mNSS result after MEF2A knockdown. (F) The step-through latency result after MEF2A knockdown. (G,H) The OPS recovery rate after MEF2A knockdown. (I-K) Western blot analysis of ERS-related proteins CHOP and GRP78 in the hippocampus at 14 days after AAV9-MEF2A RNAi microinjection, beta-actin was used as an internal control. (L-N) Western blot analysis of ERS-related proteins ERK5 and p-ERK5 in the hippocampus at 14 days after AAV9-MEF2A RNAi microinjection, beta-actin was used as an internal control. ** P < 0.01 and *** P < 0.001 using one-way ANOVA followed by Tukey's post hoc tests.