NEK6 Antibody [P9K17] | Primary Antibodies

Application: Reactivity: Human

Usage Information

Dilution
WB1:1000-1:10000

Application
WB

Reactivity
Human

Source
Rabbit Monoclonal Antibody

Storage Buffer
PBS, pH 7.2+50% Glycerol+0.05% BSA+0.01% NaN3

Storage (from the date of receipt)
-20°C (avoid freeze-thaw cycles), 2 years

Predicted MW Observed MW
36 kDa 36 kDa,53 kDa
^*Why do the predicted and actual molecular weights differ? The following reasons may explain differences between the predicted and actual protein molecular weight. Post-translational modifications(e.g., phosphorylation, glycosylation); Splice variants and isoforms; Relative charge; Multimerization.

Datasheet & SDS

Biological Description

Specificity
NEK6 Antibody [P9K17] detects endogenous levels of total NEK6 protein.

Clone
P9K17

Synonym(s)
Serine/threonine-protein kinase Nek6, Never in mitosis A-related kinase 6, Protein kinase SID6-1512, NimA-related protein kinase 6, NEK6

Background
NIMA‑related kinase 6 (NEK6) is a serine/threonine protein kinase of the NIMA family that functions in mitotic cell cycle control, where it is required for progression through metaphase, proper chromosome segregation, robust mitotic spindle formation, and completion of cytokinesis. The kinase has a mostly globular catalytic domain with a short, conformationally flexible N‑terminal extension and lacks large accessory regulatory domains, and it behaves as a monomeric enzyme that depends on upstream activating kinases rather than stable multiprotein complexes for its core activity. Activation of NEK6 occurs downstream of NEK9, which is itself activated by CDK1‑ and PLK1‑dependent phosphorylation and then phosphorylates NEK6 on defined serine residues, establishing a NEK9–NEK6 kinase cascade that operates during G2/M to promote mitotic entry and progression. NEK6 phosphorylates a range of substrates involved in spindle dynamics and chromosome movement, including the kinesin KIF11/EG5 and β‑tubulin, and these phosphorylation events support assembly and maintenance of a bipolar mitotic spindle and efficient chromosome congression. The kinase also targets regulatory and chromatin‑associated proteins such as histones H1 and H3, transcriptional regulators, and factors linked to translational control, integrating its activity with broader control of gene expression and cell cycle–related transcriptional programs. NEK6 participates in the DNA damage response by contributing to G2/M phase arrest after genotoxic stress, and inhibition or loss of NEK6 activity under these conditions is associated with mitotic failure and apoptosis, indicating that NEK6 activity is necessary for the survival of dividing cells under checkpoint control. Expression of NEK6 is elevated in several human cancers, and NEK6 activity associates with suppression of p53‑dependent senescence, linking this kinase to oncogenic pathways that favor continued proliferation and resistance to growth arrest. Across tumor contexts, NEK6 expression correlates with pathways such as PI3K–Akt, cell cycle progression, and actin cytoskeleton regulation, and NEK6‑high tumors show transcriptional signatures consistent with enhanced mitotic activity and altered cell adhesion and migration.

Background

NIMA‑related kinase 6 (NEK6) is a serine/threonine protein kinase of the NIMA family that functions in mitotic cell cycle control, where it is required for progression through metaphase, proper chromosome segregation, robust mitotic spindle formation, and completion of cytokinesis. The kinase has a mostly globular catalytic domain with a short, conformationally flexible N‑terminal extension and lacks large accessory regulatory domains, and it behaves as a monomeric enzyme that depends on upstream activating kinases rather than stable multiprotein complexes for its core activity. Activation of NEK6 occurs downstream of NEK9, which is itself activated by CDK1‑ and PLK1‑dependent phosphorylation and then phosphorylates NEK6 on defined serine residues, establishing a NEK9–NEK6 kinase cascade that operates during G2/M to promote mitotic entry and progression. NEK6 phosphorylates a range of substrates involved in spindle dynamics and chromosome movement, including the kinesin KIF11/EG5 and β‑tubulin, and these phosphorylation events support assembly and maintenance of a bipolar mitotic spindle and efficient chromosome congression. The kinase also targets regulatory and chromatin‑associated proteins such as histones H1 and H3, transcriptional regulators, and factors linked to translational control, integrating its activity with broader control of gene expression and cell cycle–related transcriptional programs. NEK6 participates in the DNA damage response by contributing to G2/M phase arrest after genotoxic stress, and inhibition or loss of NEK6 activity under these conditions is associated with mitotic failure and apoptosis, indicating that NEK6 activity is necessary for the survival of dividing cells under checkpoint control. Expression of NEK6 is elevated in several human cancers, and NEK6 activity associates with suppression of p53‑dependent senescence, linking this kinase to oncogenic pathways that favor continued proliferation and resistance to growth arrest. Across tumor contexts, NEK6 expression correlates with pathways such as PI3K–Akt, cell cycle progression, and actin cytoskeleton regulation, and NEK6‑high tumors show transcriptional signatures consistent with enhanced mitotic activity and altered cell adhesion and migration.

References
https://pubmed.ncbi.nlm.nih.gov/18728393/ https://pubmed.ncbi.nlm.nih.gov/19414596/

Reference Table for Selecting PVDF Membrane Pore Size Specifications

Protein Size (kDa)	PVDF Transfer Membrane Pore Size (μm)
< 10	0.22
10-20	0.22
20-30	0.45
30-45	0.45
45-70	0.45
80-100	0.45
100-140	0.45
> 140	0.45

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Protein Size (kDa)	Separating Gel Percentage
4-40	20%
12-45	15%
10-70	12.5%
15-100	10%
25-100	8%
60-210	5%