β2 Microglobulin Antibody [D17A9]

Application: Reactivity: Mouse, Rat, Human

Lane 1: Hela, Lane 2: Hela (KO B2M), Lane 3: Mouse kidney, Lane 4: Rat kidney

Usage Information

Dilution
WB1:5000 IP1:20-1:40 IF1:100-1:250 FCM1:20-1:60

Application
WB, IP, IF, FCM

Reactivity
Mouse, Rat, 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
14 kDa 14 kDa, 12 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
β2 Microglobulin Antibody [D17A9] detects endogenous levels of total β2 Microglobulin protein.

Clone
D17A9

Synonym(s)
CDABP0092, HDCMA22P, B2M, Beta-2-microglobulin

Background
Beta‑2‑microglobulin (β2M; B2M) is a small, invariant subunit of the class I major histocompatibility complex (MHC I) that is expressed on the surface of nearly all nucleated cells and is required for the proper folding, stability, and cell‑surface expression of MHC I molecules. Within the endoplasmic reticulum, β2M noncovalently associates with the polymorphic MHC I heavy chain and undergoes an assembly process that allows loading of intracellularly derived peptides via the peptide‑loading complex, including TAP and tapasin; this β2M‑containing MHC I‑peptide complex is then transported to the plasma membrane, where it is surveyed by CD8⁺ T cells to detect infected or malignant cells. β2M also participates in the neonatal Fc receptor (FcRn) pathway, where it stabilizes and extends the half‑life of immunoglobulin‑G by enabling pH‑dependent binding and recycling of IgG, thereby linking β2M to humoral immunity and albumin‑handling physiology. β2M is filtered by the glomerulus and catabolized by proximal tubules, so serum and urinary β2M levels rise in chronic kidney disease, multiple myeloma, and some lymphoproliferative disorders, and serum β2M is used as a prognostic staging parameter in myeloma and as a marker of disease burden and immune‑activation status in other malignancies. Excess β2M can deposit in joint and connective tissues, and genetic or acquired defects in β2M or MHC I trafficking can impair immune surveillance and alter responses to infection and cancer in amyloidogenic conditions such as dialysis‑related amyloidosis.

Background

Beta‑2‑microglobulin (β2M; B2M) is a small, invariant subunit of the class I major histocompatibility complex (MHC I) that is expressed on the surface of nearly all nucleated cells and is required for the proper folding, stability, and cell‑surface expression of MHC I molecules. Within the endoplasmic reticulum, β2M noncovalently associates with the polymorphic MHC I heavy chain and undergoes an assembly process that allows loading of intracellularly derived peptides via the peptide‑loading complex, including TAP and tapasin; this β2M‑containing MHC I‑peptide complex is then transported to the plasma membrane, where it is surveyed by CD8⁺ T cells to detect infected or malignant cells. β2M also participates in the neonatal Fc receptor (FcRn) pathway, where it stabilizes and extends the half‑life of immunoglobulin‑G by enabling pH‑dependent binding and recycling of IgG, thereby linking β2M to humoral immunity and albumin‑handling physiology. β2M is filtered by the glomerulus and catabolized by proximal tubules, so serum and urinary β2M levels rise in chronic kidney disease, multiple myeloma, and some lymphoproliferative disorders, and serum β2M is used as a prognostic staging parameter in myeloma and as a marker of disease burden and immune‑activation status in other malignancies. Excess β2M can deposit in joint and connective tissues, and genetic or acquired defects in β2M or MHC I trafficking can impair immune surveillance and alter responses to infection and cancer in amyloidogenic conditions such as dialysis‑related amyloidosis.

References
https://pubmed.ncbi.nlm.nih.gov/93282/ https://pubmed.ncbi.nlm.nih.gov/28664159/

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%