NuMA Antibody [K18C4] | Primary Antibodies

Application: Reactivity: Human

Lane 1: K562, Lane 2: Hela, Lane 3: MCF7, Lane 4: Raji

Usage Information

Dilution
WB1:1000-1:10000 IHC1:250-1:500 IF1:100-1:250

Application
WB, IHC, IF

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
238 kDa

Datasheet & SDS

Biological Description

Specificity
NuMA Antibody [K18C4] detects endogenous levels of total NuMA protein.

Clone
K18C4

Synonym(s)
NMP22; NUMA; NUMA1; Nuclear mitotic apparatus protein 1; Nuclear matrix protein‑22; Nuclear mitotic apparatus protein; SP‑H antigen; NMP‑22; NuMA protein

Background
NuMA (nuclear mitotic apparatus protein), a coiled-coil microtubule-binding protein dynamically shuttling between interphase nuclei and mitotic spindle poles, orchestrates chromosome segregation, nuclear reformation, and spindle positioning across proliferating cell types. During mitosis, NuMA concentrates at minus-ends via dynein-dynactin tethering and LGN-Gαi cortical interactions, crosslinking astral microtubules to generate poleward forces that focus spindle poles and align chromosomes at the metaphase plate through regulated microtubule flux. Aurora A kinase phosphorylates NuMA to recruit Kif2A depolymerases, enhancing microtubule disassembly at poles while phase-separated NuMA droplets organize microtubule arrays independent of canonical motors; at anaphase, NuMA transitions to decondensing chromosomes, binding DNA via its C-terminus to compact the mass and exclude importins, ensuring single round nuclear reformation via chromatin-tethered microtubule aster formation. This integrates into the RanGTP gradient pathway where chromosome-proximal RCC1 generates RanGTP to release NuMA from importin-β, licensing local spindle assembly, while NuMA negatively regulates 53BP1 foci at DNA breaks by competing for H4K20me2 binding to suppress NHEJ and favor HR repair. NuMA governs symmetric neurogenic divisions in neural progenitors and ensures genomic stability in epithelial tissues, making it essential for researchers modeling aneuploidy in CRISPR organoids or quantifying spindle defects via live-cell polarity sensors. Deficiency triggers micronuclei, mitotic arrest, and synthetic lethality with APC mutations, while overexpression elongates spindles and drives multipolar mitosis in cancers. Post-translational control by SUMOylation and CDK1 phosphorylation fine-tunes its dual nuclear-mitotic roles.

Background

NuMA (nuclear mitotic apparatus protein), a coiled-coil microtubule-binding protein dynamically shuttling between interphase nuclei and mitotic spindle poles, orchestrates chromosome segregation, nuclear reformation, and spindle positioning across proliferating cell types. During mitosis, NuMA concentrates at minus-ends via dynein-dynactin tethering and LGN-Gαi cortical interactions, crosslinking astral microtubules to generate poleward forces that focus spindle poles and align chromosomes at the metaphase plate through regulated microtubule flux. Aurora A kinase phosphorylates NuMA to recruit Kif2A depolymerases, enhancing microtubule disassembly at poles while phase-separated NuMA droplets organize microtubule arrays independent of canonical motors; at anaphase, NuMA transitions to decondensing chromosomes, binding DNA via its C-terminus to compact the mass and exclude importins, ensuring single round nuclear reformation via chromatin-tethered microtubule aster formation. This integrates into the RanGTP gradient pathway where chromosome-proximal RCC1 generates RanGTP to release NuMA from importin-β, licensing local spindle assembly, while NuMA negatively regulates 53BP1 foci at DNA breaks by competing for H4K20me2 binding to suppress NHEJ and favor HR repair. NuMA governs symmetric neurogenic divisions in neural progenitors and ensures genomic stability in epithelial tissues, making it essential for researchers modeling aneuploidy in CRISPR organoids or quantifying spindle defects via live-cell polarity sensors. Deficiency triggers micronuclei, mitotic arrest, and synthetic lethality with APC mutations, while overexpression elongates spindles and drives multipolar mitosis in cancers. Post-translational control by SUMOylation and CDK1 phosphorylation fine-tunes its dual nuclear-mitotic roles.

References
https://pubmed.ncbi.nlm.nih.gov/33044554/ https://pubmed.ncbi.nlm.nih.gov/34887424/

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%