PKMYT1 Antibody (YA8105)
(Synonyms: MYT1; PPP1R126)Based on 1 Customer Validation
PKMYT1 Antibody (YA8105) is a Mouse-derived and non-conjugated IgG2a monoclonal antibody, targeting to PKMYT1.
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Host:
Mouse
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Isotype:
IgG
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Application:
WB, IHC-P, ICC/IF, FC
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Reactivity :
Human, Mouse, Rat
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Formulation:
Spplied in PBS (pH 7.3) containing 1% BSA, 50% glycerol and 0.02% sodium azide.
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Conjugation:
Non-conjugated
Applications
| Application |
WB
WB: Western Blot
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IHC-P
IHC-P: Immunohistochemistry-Paraffin
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ICC/IF
ICC/IF: Immunocytochemistry/
Immunofluorescence |
FC
FC: Flow Cytometry
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|---|---|---|---|---|
| Dilution Ratio | 1:500 | 1:50-250 | 1:100-250 | 1:100 |
Product Details
PKMYT1 Antibody (YA8105) is a Mouse-derived and non-conjugated IgG2a monoclonal antibody, targeting to PKMYT1.
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Host Mouse
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Clonality Monoclonal
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Species ReactivityHuman, Mouse, Rat
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Calculated Molecular Weight Predicted band size: 54.3 kDa
Full length human recombinant protein of human PKMYT1 produced in HEK293T cell.
Endogenous
Affinity purified
Non-conjugated
Unmodified
IgG
Product Properties
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Appearance
Solution
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Formulation
Spplied in PBS (pH 7.3) containing 1% BSA, 50% glycerol and 0.02% sodium azide.
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Concentration
Batch-dependent, Please check the COA for the concentration of each lot. Check Lot Concentration
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Storage & Stability
Stored at -20°C for 1 year. Avoid repeated freeze / thaw cycles.
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Shipping
Shipping with blue ice.
Background
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Function
PKMYT1 (protein kinase, membrane associated tyrosine/threonine 1) is a member of the WEE kinase family that functions as a key negative regulator of CDK1 activity and mitotic entry, thereby contributing to cell-cycle control and genomic stability[1]. Mechanistically, PKMYT1 participates in the G2/M checkpoint, where WEE-family kinases maintain inhibitory control over CDK1 to prevent premature progression into mitosis under conditions requiring cell-cycle surveillance[1][2]. Through this checkpoint-regulatory role, PKMYT1 supports proper mitotic timing and helps preserve genetic integrity in proliferating cells[1][2]. In cancer biology, increasing evidence indicates that tumor cells can become highly dependent on WEE-family kinase activity, including PKMYT1, to tolerate replication stress and DNA damage, making this pathway a relevant target for therapeutic investigation[1][2]. Studies in colorectal cancer have shown elevated PKMYT1 expression and demonstrated that PKMYT1 silencing impairs cellular proliferation, cell-cycle progression, migration, and invasion, supporting a role in tumor development and maintenance[3]. Compared with the related isoform WEE1, which has received substantially greater research attention, PKMYT1 remains a comparatively underexplored member of the WEE kinase family despite sharing critical functions in regulating mitotic control[4]. For experimental applications, PKMYT1 inhibitors have emerged as valuable tools for investigating G2/M checkpoint dependence, and inhibition of PKMYT1 can promote checkpoint override, premature mitotic entry, and mitotic cell death in cancer models, supporting its development as a potential therapeutic target[1].
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Subcellular Localization
Endoplasmic reticulum membrane,Golgi apparatus membrane
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Isoforms & Post-Translational Modification
Q99640 has four isomers: Q99640-1: 54521 Da (predicted); Q99640-2: 52146 Da (predicted); Q99640-3: 53542 Da (predicted); Q99640-4: 47284 Da (predicted).
Autophosphorylated -
Subunit
Interacts with CDC2-CCNB1 complex
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SwissProt ID
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Synonyms
MYT1; PPP1R126
Documentation
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Data Sheet (260 KB)
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SDS (251 KB)
- English - EN (251 KB)
- Français - FR (251 KB)
- Deutsch - DE (251 KB)
- Norwegian - NO (251 KB)
- Español - ES (251 KB)
- Swedish - SV (251 KB)
- Italian - IT (251 KB)
- Korean - KR (251 KB)
- Portuguese - PT (251 KB)
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User Guide for Antibodies (1077 KB)
References
[1]. Ghelli Luserna di Rorà A, et al. A WEE1 family business: regulation of mitosis, cancer progression, and therapeutic target. J Hematol Oncol. 2020 Sep 21;13(1):126. [Content Brief]
[3]. Zhang Y, et al. Exploring PKMYT1 as a potential marker for colorectal cancer progression through bioinformatics analyses and experimental validation. Sci Rep. 2025 Sep 26;15(1):33016. [Content Brief]