FMRP Antibody [C2F21] | Primary Antibodies

Application: Reactivity: Mouse, Rat, Human

Lane 1: Hela, Lane 2: 3T3, Lane 3: PC12, Lane 4: Mouse brain

Usage Information

Dilution
WB1:1000 IP1:30 IHC1:10000 IF1:50 FCM1:500

Application
WB, IP, IHC, 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
71 kDa 70-77 kDa, 80 kDa
^*Why do the predicted and actual molecular weights differ? The following reasons may explain differences between the predicted and actual protein molecular weight.

Positive Control	Mouse cerebrum tissue; Mouse hippocampus tissue; Mouse spinal cord tissue; Rat cerebrum tissue; Rat cerebellum; Rat spinal cord tissue; Rat hippocampus tissue; Rat brain frozen tissue; Rat testis frozen tissue; NIH/3T3 cells; PC-12 cells; HAP1 cells; A549 cells; HeLa cells; C2C12 cells
Negative Control	Mouse heart tissue; Human brain cells

Datasheet & SDS

Biological Description

Specificity
FMRP Antibody [C2F21] detects endogenous levels of total FMRP protein.

Clone
C2F21

Synonym(s)
Fragile X messenger ribonucleoprotein 1; Fragile X messenger ribonucleoprotein; Protein FMR-1; FMRP; FMR1

Background
FMRP (Fragile X Messenger Ribonucleoprotein), encoded by FMR1 and absent in Fragile X syndrome (FXS), the most common inherited intellectual disability and a leading monogenic autism cause, features an N-terminal tandem Agenet/Tudor domain (residues 1–94/98–202) mediating protein interactions (including CYFIP1/2 binding and methylated histone H4 recognition), flanked by a non-canonical KH0 module (aa ~15–91), two canonical K-homology domains KH1 (aa 202–269) and KH2 (aa 285–389) that selectively bind G-quadruplex (G4) and kissing complex stem-loop RNA structures (such as those in MAP1B, SHANK3, and CYFIP mRNAs) via conserved GXXG loops. Its C-terminal RGG box (aa 590–632), methylated at arginine residues, further enhances RNA affinity and enables nuclear shuttling through an NLS (aa 219–222) and NES (aa 462–479), while Ser500 phosphorylation modulates ribosome association. Predominantly cytoplasmic in neurons, FMRP assembles into over 1,000 mRNP granules transported along microtubules via kinesin/dynein to dendrites and synapses, where it represses translation of synaptic plasticity mRNAs (PSD-95, GluA1/2, Arc, MAP1B) by stalling 80S ribosomes at initiation. KH2-domain binding to BCS1L-like kissing loops blocks eIF4E/eIF4AI and recruits CYFIP1 to inhibit eIF4E–cap interaction, while Tudor domains recruit miRISC (Ago2) for miRNA-mediated silencing and induce stress granule/P-body partitioning under mGluR-LTP stimuli. FMRP can also activate translation of select targets (like GIRK2 via internal initiation), and Ser500 phosphorylation switches its activity from polysome repression to activation; domain synergy (KH + C-term) is critical for puncta formation and microtubule association essential for local protein synthesis. In FXS, FMR1 CGG expansions (>200 repeats) lead to CpG island hypermethylation and FMRP silencing, resulting in excessive protein synthesis, dendritic spine dysmaturation, seizures, and macroorchidism, while KH2 mutations (I304N/G266E) disrupt G4/kissing-loop selectivity and cause FXS-like phenotypes. Additionally, upregulated FMRP in cancers (e.g., glioma) stabilizes oncogenic mRNAs, and its dysregulation is implicated in neurodevelopmental disorders, including schizophrenia, via impaired mGluR-dependent LTD.

Background

FMRP (Fragile X Messenger Ribonucleoprotein), encoded by FMR1 and absent in Fragile X syndrome (FXS), the most common inherited intellectual disability and a leading monogenic autism cause, features an N-terminal tandem Agenet/Tudor domain (residues 1–94/98–202) mediating protein interactions (including CYFIP1/2 binding and methylated histone H4 recognition), flanked by a non-canonical KH0 module (aa ~15–91), two canonical K-homology domains KH1 (aa 202–269) and KH2 (aa 285–389) that selectively bind G-quadruplex (G4) and kissing complex stem-loop RNA structures (such as those in MAP1B, SHANK3, and CYFIP mRNAs) via conserved GXXG loops. Its C-terminal RGG box (aa 590–632), methylated at arginine residues, further enhances RNA affinity and enables nuclear shuttling through an NLS (aa 219–222) and NES (aa 462–479), while Ser500 phosphorylation modulates ribosome association. Predominantly cytoplasmic in neurons, FMRP assembles into over 1,000 mRNP granules transported along microtubules via kinesin/dynein to dendrites and synapses, where it represses translation of synaptic plasticity mRNAs (PSD-95, GluA1/2, Arc, MAP1B) by stalling 80S ribosomes at initiation. KH2-domain binding to BCS1L-like kissing loops blocks eIF4E/eIF4AI and recruits CYFIP1 to inhibit eIF4E–cap interaction, while Tudor domains recruit miRISC (Ago2) for miRNA-mediated silencing and induce stress granule/P-body partitioning under mGluR-LTP stimuli. FMRP can also activate translation of select targets (like GIRK2 via internal initiation), and Ser500 phosphorylation switches its activity from polysome repression to activation; domain synergy (KH + C-term) is critical for puncta formation and microtubule association essential for local protein synthesis. In FXS, FMR1 CGG expansions (>200 repeats) lead to CpG island hypermethylation and FMRP silencing, resulting in excessive protein synthesis, dendritic spine dysmaturation, seizures, and macroorchidism, while KH2 mutations (I304N/G266E) disrupt G4/kissing-loop selectivity and cause FXS-like phenotypes. Additionally, upregulated FMRP in cancers (e.g., glioma) stabilizes oncogenic mRNAs, and its dysregulation is implicated in neurodevelopmental disorders, including schizophrenia, via impaired mGluR-dependent LTD.

References
https://pubmed.ncbi.nlm.nih.gov/32343993/ https://pubmed.ncbi.nlm.nih.gov/25416280/

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%