MX1 Antibody [C7P8] | Primary Antibodies

Application: Reactivity: Human

Lane 1: Hela, Lane 2: Hela (hIFN-α1, 100 ng/ml, 16 h)

Usage Information

Dilution
WB1:1000 - 1:2000 IP1:40 - 1:1000 IF1:250 FCM1:500

Application
WB, IP, IF, FCM

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
76 kDa 76 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
MX1 Antibody [C7P8] detects endogenous levels of total MX1 protein.

Clone
C7P8

Synonym(s)
Interferon-induced GTP-binding protein Mx1, Interferon-induced protein p78, Interferon-regulated resistance GTP-binding protein MxA, Myxoma resistance protein 1, Myxovirus resistance protein 1, IFI-78K, MX1

Background
MX1 (myxovirus resistance protein 1) is an interferon‑inducible dynamin‑like large GTPase of the innate immune system that acts as a broad antiviral effector downstream of type I and type III interferon signaling and contributes to cell‑intrinsic restriction of diverse RNA and some DNA viruses. The protein contains an N‑terminal GTPase domain, a central bundle‑signaling or stalk region, and a C‑terminal GTPase effector domain, which together support nucleotide binding and hydrolysis, higher‑order oligomerization, and association with intracellular membranes and viral components in a manner typical for the dynamin superfamily. MX1 expression is strongly induced by interferon‑stimulated transcriptional programs and localizes to characteristic cytoplasmic or perinuclear structures where it encounters incoming viral nucleocapsids or ribonucleoprotein complexes and exerts antiviral functions that depend on GTP hydrolysis‑driven conformational changes and assembly into oligomeric scaffolds. Antiviral activity against orthomyxoviruses such as influenza A involves binding to viral ribonucleoprotein complexes and interference with functional assembly of the viral polymerase and nucleoprotein, leading to a block of primary transcription and early replication steps and a sharp reduction in productive infection. MX1 also targets other enveloped and non‑enveloped RNA viruses, including members of bunyaviridae and rhabdoviridae, by interacting with nucleocapsid proteins and altering their trafficking, uncoating, or nuclear import, thereby preventing completion of the replication cycle and reducing progeny virus production. Induction of MX1 expression forms part of a wider interferon‑stimulated gene network, but MX1 makes a non‑redundant contribution to resistance, as its presence defines a barrier to infection by sensitive viruses and its absence or low expression correlates with increased viral replication and more severe disease outcomes in experimental systems and natural infection settings.

Background

MX1 (myxovirus resistance protein 1) is an interferon‑inducible dynamin‑like large GTPase of the innate immune system that acts as a broad antiviral effector downstream of type I and type III interferon signaling and contributes to cell‑intrinsic restriction of diverse RNA and some DNA viruses. The protein contains an N‑terminal GTPase domain, a central bundle‑signaling or stalk region, and a C‑terminal GTPase effector domain, which together support nucleotide binding and hydrolysis, higher‑order oligomerization, and association with intracellular membranes and viral components in a manner typical for the dynamin superfamily. MX1 expression is strongly induced by interferon‑stimulated transcriptional programs and localizes to characteristic cytoplasmic or perinuclear structures where it encounters incoming viral nucleocapsids or ribonucleoprotein complexes and exerts antiviral functions that depend on GTP hydrolysis‑driven conformational changes and assembly into oligomeric scaffolds. Antiviral activity against orthomyxoviruses such as influenza A involves binding to viral ribonucleoprotein complexes and interference with functional assembly of the viral polymerase and nucleoprotein, leading to a block of primary transcription and early replication steps and a sharp reduction in productive infection. MX1 also targets other enveloped and non‑enveloped RNA viruses, including members of bunyaviridae and rhabdoviridae, by interacting with nucleocapsid proteins and altering their trafficking, uncoating, or nuclear import, thereby preventing completion of the replication cycle and reducing progeny virus production. Induction of MX1 expression forms part of a wider interferon‑stimulated gene network, but MX1 makes a non‑redundant contribution to resistance, as its presence defines a barrier to infection by sensitive viruses and its absence or low expression correlates with increased viral replication and more severe disease outcomes in experimental systems and natural infection settings.

References
https://pubmed.ncbi.nlm.nih.gov/23015724/ https://pubmed.ncbi.nlm.nih.gov/24296571/

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%