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AB5686

Anti-ERK5 (phospho T219 + Y221) antibody

3

(2 Reviews)

|

(11 Publications)

Rabbit Polyclonal ERK5 phospho T219 + Y221 antibody. Suitable for WB and reacts with Human samples. Cited in 11 publications. Immunogen corresponding to Synthetic Peptide within Human MAPK7 pY220 + T218.

View Alternative Names

BMK1, ERK5, PRKM7, MAPK7, Mitogen-activated protein kinase 7, MAP kinase 7, MAPK 7, Big MAP kinase 1, Extracellular signal-regulated kinase 5, BMK-1, ERK-5

1 Images
Western blot - Anti-ERK5 (phospho T219 + Y221) antibody (AB5686)
  • WB

Unknown

Western blot - Anti-ERK5 (phospho T219 + Y221) antibody (AB5686)

Peptide Competition :
Extracts prepared from HEK293 cells transiently transfected with plasmids expressing ERK5 kinase domain (ERK5kin) and constitutively activated MEK5D-D were resolved by SDS-PAGE on a 10% polyacrylamide gel and transferred to PVDF. Membranes were blocked with a 5% BSA TBST buffer overnight at 4oC, then were incubated with the ab5686 antibody for two hours at room temperature in a 3% BSATBST buffer, following prior incubation with : no peptide (1), the non-phosphopeptide corresponding to the immunogen (2), a generic phosphothreonine-containing peptide (3), a generic phosphotyrosine-containing peptide (4), the phosphopeptide derived from the corresponding region of ERK1&2 (5), or, the phosphopeptide immunogen (6). After washing, membranes were incubated with goat F(ab’ 2 anti-rabbit IgG alkaline phosphatase conjugate and bands were detected using the Tropix WesternStarTM detection method. The data show that while there is some cross-reactivity with ERK1&

All lanes:

Western blot - Anti-ERK5 (phospho T219 + Y221) antibody (ab5686)

Predicted band size: 88 kDa

false

Key facts

Host species

Rabbit

Clonality

Polyclonal

Isotype

IgG

Carrier free

No

Reacts with

Human

Applications

WB

applications

Immunogen

Synthetic Peptide within Human MAPK7 pY220 + T218. The exact immunogen used to generate this antibody is proprietary information.

Q13164

Specificity

Some cross-reactivity is observed with endogenous ERK1 and 2 (44 and 42 kDa, respectively) due to the high levels of expression and activation of this protein typically observed with most cell types.

Reactivity data

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Properties and storage information

Form
Liquid
Purification technique
Affinity purification Immunogen
Purification notes
The antibody has been negatively preadsorbed using a non-phosphopeptide corresponding to the site of phosphorylation to remove antibody that is reactive with non-phosphorylated ERK5. The final product is generated by affinity chromatography using an ERK5-derived peptide that is phosphorylated at threonine 218 and tyrosine 220.
Storage buffer
pH: 7.3 Preservative: 0.05% Sodium azide Constituents: PBS, 50% Glycerol (glycerin, glycerine), 0.1% BSA
Shipped at conditions
Blue Ice
Appropriate short-term storage conditions
+4°C
Appropriate long-term storage conditions
-20°C
Aliquoting information
Upon delivery aliquot
Storage information
Avoid freeze / thaw cycle

Supplementary information

This supplementary information is collated from multiple sources and compiled automatically.

ERK5 also known as big MAP kinase 1 (BMK1) is an enzyme that functions as a protein-serine/threonine kinase within the MAP kinase family. It has a molecular weight of approximately 120 kDa. ERK5 is expressed in various tissues including the brain heart and lungs with notable expression in endothelial cells. The protein plays a mechanical role in signal transduction processes which it achieves by transmitting signals from extracellular sources to the cellular nucleus facilitating the regulation of gene expression.
Biological function summary

ERK5 influences cellular functions through its role in promoting cell proliferation and differentiation. It serves as part of a signaling complex that includes the MAP kinase kinase 5 (MEK5). This interaction allows ERK5 to phosphorylate and subsequently activate target substrates such as transcription factors promoting cellular responses necessary for development and survival. ERK5 also plays a role in the response to oxidative stress which contributes to its impact on survival pathways and cellular stress responses.

Pathways

ERK5 acts within the MAPK signaling cascade and is linked to the ERK/MAPK pathway and the phosphoinositide 3-kinase (PI3K) pathway. Within these pathways ERK5 interacts with other MAP kinases and regulatory proteins such as Ras and Raf contributing to a wide range of cellular processes including growth migration and survival. Through these interactions ERK5 influences cellular dynamics and mediates responses to growth factors and stress stimuli.

Abnormal activity of ERK5 has been implicated in various conditions including cardiovascular disease and cancer. Elevated ERK5 signaling can promote tumor progression and metastasis in certain cancers by enhancing tumor cell proliferation and survival. In cardiovascular disorders ERK5 interacts with proteins like calcium/calmodulin-dependent protein kinase II (CaMKII) influencing pathological cardiac remodeling and hypertrophy. These associations highlight ERK5's impact on disease mechanisms and highlight its potential as a therapeutic target.

Product protocols

For this product, it's our understanding that no specific protocols are required. You can visit:

Target data

Plays a role in various cellular processes such as proliferation, differentiation and cell survival. The upstream activator of MAPK7 is the MAPK kinase MAP2K5. Upon activation, it translocates to the nucleus and phosphorylates various downstream targets including MEF2C. EGF activates MAPK7 through a Ras-independent and MAP2K5-dependent pathway. As part of the MAPK/ERK signaling pathway, acts as a negative regulator of apoptosis in cardiomyocytes via interaction with STUB1/CHIP and promotion of STUB1-mediated ubiquitination and degradation of ICER-type isoforms of CREM (By similarity). May have a role in muscle cell differentiation. May be important for endothelial function and maintenance of blood vessel integrity. MAP2K5 and MAPK7 interact specifically with one another and not with MEK1/ERK1 or MEK2/ERK2 pathways. Phosphorylates SGK1 at Ser-78 and this is required for growth factor-induced cell cycle progression. Involved in the regulation of p53/TP53 by disrupting the PML-MDM2 interaction.
See full target information MAPK7 pT219 + Y221

Publications (11)

Recent publications for all applications. Explore the full list and refine your search

International journal of molecular medicine 53: PubMed38214344

2024

Regulator of G protein signalling 18 promotes osteocyte proliferation by activating the extracellular signal‑regulated kinase signalling pathway.

Applications

Unspecified application

Species

Unspecified reactive species

Yong Meng,Si-Qiang Qiu,Qiang Wang,Jin-Liang Zuo

Diabetes, obesity & metabolism 24:1721-1733 PubMed35546452

2022

Polarized macrophages promote gestational beta cell growth through extracellular signal-regulated kinase 5 signalling.

Applications

Unspecified application

Species

Unspecified reactive species

Yinan Jiang,Apeng Chen,Diana Kline,Qun Liu,Jie Ma,Yan Wang,Ting Zhang,Jieqi Qian,Laura Nelson,Krishna Prasadan,Baoli Hu,George K Gittes,Xiangwei Xiao

Aging 13:16088-16104 PubMed34176788

2021

High glucose exacerbates neuroinflammation and apoptosis at the intermediate stage after post-traumatic brain injury.

Applications

Unspecified application

Species

Unspecified reactive species

Wenqian Zhang,Jun Hong,Wencheng Zheng,Aijun Liu,Ying Yang

Journal of neuroscience research 99:1666-1688 PubMed33729593

2021

Extracellular signal-regulated kinases 2 (Erk2) and Erk5 in the central nervous system differentially contribute to central sensitization in male mice.

Applications

Unspecified application

Species

Unspecified reactive species

Fumihiro Matsuura,Yasushi Satoh,Sayako Itakura,Toru Morohashi,Masanori Kawaguchi,Tetsuya Takahashi,Koji Iwanaga,Hayato Terashima,Yasushi Kobayashi,Xin Wang,Toshiaki Ishizuka,Shogo Endo,Takehiko Ikeda

Experimental and therapeutic medicine 21:470 PubMed33767765

2021

Proof-of-concept study investigating the role of S100P-RAGE in nasopharyngeal carcinoma.

Applications

Unspecified application

Species

Unspecified reactive species

Chengyu Wang,Xueqiao Wang,Angxuan Han,Yuhao Wang,Hui Jiang

Journal of cellular and molecular medicine 25:3803-3815 PubMed33621420

2021

Isoflurane post-conditioning contributes to anti-apoptotic effect after cerebral ischaemia in rats through the ERK5/MEF2D signaling pathway.

Applications

Unspecified application

Species

Unspecified reactive species

Qingtong Zhang,Jiangwen Yin,Feng Xu,Jingwen Zhai,Jieting Yin,Mingyue Ge,Wenyi Zhou,Nian Li,Xinlei Qin,Yan Li,Sheng Wang

Journal of trace elements in medicine and biology 61:126546 PubMed32480051

2020

Involvement of MEK5/ERK5 signaling pathway in manganese-induced cell injury in dopaminergic MN9D cells.

Applications

Unspecified application

Species

Unspecified reactive species

Hongwei Ding,Feng Wang,Liyu Su,Lan Zhao,Binli Hu,Wei Zheng,Shengtao Yao,Yan Li

BMC cancer 19:297 PubMed30940124

2019

LncRNA ENST00000539653 acts as an oncogenic factor via MAPK signalling in papillary thyroid cancer.

Applications

Unspecified application

Species

Unspecified reactive species

Bin Song,Rurun Li,Zhihua Zuo,Juan Tan,Ling Liu,Dafa Ding,Yibing Lu,Dawei Hou

Journal of cellular biochemistry 120:9964-9978 PubMed30582202

2018

MicroRNA-329-mediated PTTG1 downregulation inactivates the MAPK signaling pathway to suppress cell proliferation and tumor growth in cholangiocarcinoma.

Applications

Unspecified application

Species

Unspecified reactive species

Zhi-Gao Hu,Chao-Wen Zheng,Hui-Zhao Su,Yong-Lian Zeng,Cheng-Jie Lin,Zhen-Ya Guo,Fu-Di Zhong,Guan-Dou Yuan,Song-Qing He

Journal of cellular biochemistry 120:1407-1419 PubMed30335886

2018

Retracted: EBF1 gene promotes the proliferation and inhibits the apoptosis of bone marrow CD34+ cells in patients with myelodysplastic syndrome through negative regulation of mitogen-activated protein kinase axis.

Applications

Unspecified application

Species

Unspecified reactive species

Shuang Hou,Jie Hao,Yan-Yu Wang,Bing-Bing Zhao,Gong-Wei Xiao,Yan-Qing Li,Xi Liu,Zhi-Lan Zou,Ye Yao,Hong Xiong
View all publications

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