S100B Antibody [P12F20] | Primary Antibodies

Application: Reactivity: Human, Mouse, Rat

Lane 1: SK-MEL-28

Usage Information

Dilution
WB1:1000 IHC1:100-1:400 IF1:800-1:1600

Application
WB, IHC, IF

Reactivity
Human, Mouse, Rat

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
10 kDa

Datasheet & SDS

Biological Description

Specificity
S100B Antibody [P12F20] detects endogenous levels of total S100B protein.

Clone
P12F20

Synonym(s)
Protein S100-B; S-100 protein beta chain; S-100 protein subunit beta; S100 calcium-binding protein B; S100B

Background
S100B belongs to the S100 family of EF-hand calcium-binding proteins and serves primarily as an intracellular regulator and extracellular signaling molecule abundant in astrocytes and oligodendrocytes of the central nervous system. It consists of two EF-hand motifs per monomer that form antiparallel homodimers upon calcium binding, enabling interaction with diverse targets through conformational changes that expose hydrophobic surfaces. S100B modulates cytoskeletal dynamics by binding F-actin and microtubule-associated proteins, promoting stress fiber disassembly and membrane ruffling via inhibition of PKC phosphorylation, while also influencing energy metabolism and Ca2+ homeostasis to regulate astrocyte proliferation, differentiation, and migration. S100B acts in a dose-dependent manner through RAGE receptor ligation, triggering at low physiological levels Ras/MEK/ERK/NF-κB/Bcl-2 signaling for neuroprotection, neurite outgrowth, and astrocyte proliferation, but at high pathological concentrations hyperactivating ERK with ROS overproduction to induce neuronal apoptosis; this biphasic action extends to RAGE/p38MAPK/pAkt/mTOR/HIF1α pathways that upregulate VEGF and NO while suppressing p53 in cancer cells. S100B maintains glial shape and motility critical for blood-brain barrier integrity and synaptic support, positioning it as a key target for studying astrocyte-oligodendrocyte interactions in development and repair where calcium flux dictates cellular responses. Its expression in gray matter protoplasmic astrocytes and white matter oligodendrocytes supports tissue-specific roles in myelination and neuroinflammation modulation. Dysregulation with chronic elevation promotes tumor angiogenesis and invasion in colorectal cancer via proinflammatory NF-κB activation.

Background

S100B belongs to the S100 family of EF-hand calcium-binding proteins and serves primarily as an intracellular regulator and extracellular signaling molecule abundant in astrocytes and oligodendrocytes of the central nervous system. It consists of two EF-hand motifs per monomer that form antiparallel homodimers upon calcium binding, enabling interaction with diverse targets through conformational changes that expose hydrophobic surfaces. S100B modulates cytoskeletal dynamics by binding F-actin and microtubule-associated proteins, promoting stress fiber disassembly and membrane ruffling via inhibition of PKC phosphorylation, while also influencing energy metabolism and Ca2+ homeostasis to regulate astrocyte proliferation, differentiation, and migration. S100B acts in a dose-dependent manner through RAGE receptor ligation, triggering at low physiological levels Ras/MEK/ERK/NF-κB/Bcl-2 signaling for neuroprotection, neurite outgrowth, and astrocyte proliferation, but at high pathological concentrations hyperactivating ERK with ROS overproduction to induce neuronal apoptosis; this biphasic action extends to RAGE/p38MAPK/pAkt/mTOR/HIF1α pathways that upregulate VEGF and NO while suppressing p53 in cancer cells. S100B maintains glial shape and motility critical for blood-brain barrier integrity and synaptic support, positioning it as a key target for studying astrocyte-oligodendrocyte interactions in development and repair where calcium flux dictates cellular responses. Its expression in gray matter protoplasmic astrocytes and white matter oligodendrocytes supports tissue-specific roles in myelination and neuroinflammation modulation. Dysregulation with chronic elevation promotes tumor angiogenesis and invasion in colorectal cancer via proinflammatory NF-κB activation.

References
https://pubmed.ncbi.nlm.nih.gov/31266264/ https://pubmed.ncbi.nlm.nih.gov/19147496/

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%