Neurofibromin 1 Antibody [J9P10]

Application: Reactivity: Human, Mouse, Rat, Monkey

Usage Information

Dilution
WB1:1000 IP1:50

Application
WB, IP

Reactivity
Human, Mouse, Rat, Monkey

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
320 kDa

Positive Control	HeLa cells; A204 cells
Negative Control

Datasheet & SDS

Biological Description

Specificity
Neurofibromin 1 Antibody [J9P10] detects endogenous levels of total Neurofibromin 1 protein.

Clone
J9P10

Synonym(s)
Neurofibromin; Neurofibromatosis-related protein NF-1; Neurofibromin truncated; NF1

Background
Neurofibromin 1, encoded by the tumor suppressor NF1 gene, is a large, multifunctional Ras GTPase-activating protein (RasGAP) crucial for downregulating Ras signaling in neurons, Schwann cells, and oligodendrocytes. It is characterized by an N-terminal cysteine-serine-rich domain, a central GAP-related domain (GRD) with a catalytic arginine finger, a Sec14-PH phospholipid-binding motif, and a C-terminal domain. Neurofibromin accelerates the hydrolysis of GTP to GDP on Ras, effectively shutting off the Raf/MEK/ERK MAPK pathway to restrain cell proliferation and regulate differentiation. It also modulates cAMP/PKA signaling via adenylate cyclase, interacts with microtubules, and partners with proteins like SPRED1 and ABI1 to regulate the actin cytoskeleton. Loss-of-function NF1 mutations, causing neurofibromatosis type 1, lead to hyperactive Ras, contributing to benign plexiform neurofibromas, malignant peripheral nerve sheath tumors (MPNST), gliomas, and various developmental abnormalities. Somatic NF1 mutations are frequently found in sporadic cancers, including melanoma, glioblastoma, and non-small cell lung cancer, where they drive tumor progression and confer resistance to therapy due to uncontrolled Ras-mediated signaling.

Background

Neurofibromin 1, encoded by the tumor suppressor NF1 gene, is a large, multifunctional Ras GTPase-activating protein (RasGAP) crucial for downregulating Ras signaling in neurons, Schwann cells, and oligodendrocytes. It is characterized by an N-terminal cysteine-serine-rich domain, a central GAP-related domain (GRD) with a catalytic arginine finger, a Sec14-PH phospholipid-binding motif, and a C-terminal domain. Neurofibromin accelerates the hydrolysis of GTP to GDP on Ras, effectively shutting off the Raf/MEK/ERK MAPK pathway to restrain cell proliferation and regulate differentiation. It also modulates cAMP/PKA signaling via adenylate cyclase, interacts with microtubules, and partners with proteins like SPRED1 and ABI1 to regulate the actin cytoskeleton. Loss-of-function NF1 mutations, causing neurofibromatosis type 1, lead to hyperactive Ras, contributing to benign plexiform neurofibromas, malignant peripheral nerve sheath tumors (MPNST), gliomas, and various developmental abnormalities. Somatic NF1 mutations are frequently found in sporadic cancers, including melanoma, glioblastoma, and non-small cell lung cancer, where they drive tumor progression and confer resistance to therapy due to uncontrolled Ras-mediated signaling.

References
https://pubmed.ncbi.nlm.nih.gov/33121128/ https://pubmed.ncbi.nlm.nih.gov/25877329/

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%