Product: Phospho-FUNDC1 (Ser17) antibody
Catalog: AF0001
Description: Rabbit polyclonal antibody to Phospho-FUNDC1 (Ser17)
Application: WB
Reactivity: Human
Prediction: Pig, Bovine, Horse, Sheep, Rabbit, Dog, Chicken
Mol.Wt.: 17KD; 17kD(Calculated).
Uniprot: Q8IVP5
RRID: AB_2846773

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Product Info

WB 1:500-1:2000
*The optimal dilutions should be determined by the end user.

WB: For western blot detection of denatured protein samples. IHC: For immunohistochemical detection of paraffin sections (IHC-p) or frozen sections (IHC-f) of tissue samples. IF/ICC: For immunofluorescence detection of cell samples. ELISA(peptide): For ELISA detection of antigenic peptide.

Pig(100%), Bovine(100%), Horse(100%), Sheep(100%), Rabbit(100%), Dog(88%), Chicken(100%)
Phospho-FUNDC1 (Ser17) antibody detects endogenous levels of FUNDC1 only when phosphorylated at Serine 17.
Cite Format: Affinity Biosciences Cat# AF0001, RRID:AB_2846773.
The antibody is from purified rabbit serum by affinity purification via sequential chromatography on phospho-peptide and non-phospho-peptide affinity columns.
Rabbit IgG in phosphate buffered saline , pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol. Store at -20 °C. Stable for 12 months from date of receipt.


FUN14 domain containing 1; FUN14 domain containing protein 1; FUN14 domain-containing protein 1; FUND1_HUMAN; fundc1;



Widely expressed.




Score>80(red) has high confidence and is suggested to be used for WB detection. *The prediction model is mainly based on the alignment of immunogen sequences, the results are for reference only, not as the basis of quality assurance.

Model Confidence:
High(score>80) Medium(80>score>50) Low(score<50) No confidence

PTMs - Q8IVP5 As Substrate

Site PTM Type Enzyme
Y11 Phosphorylation
S13 Phosphorylation
S17 Phosphorylation
Y18 Phosphorylation
S40 Phosphorylation
S41 Phosphorylation
K119 Ubiquitination

Research Backgrounds


Acts as an activator of hypoxia-induced mitophagy, an important mechanism for mitochondrial quality control.


Phosphorylation at Tyr-18 by SRC inhibits activation of mitophagy. Following hypoxia, dephosphorylated at Tyr-18, leading to interaction with MAP1 LC3 family proteins and triggering mitophagy.

Subcellular Location:

Mitochondrion outer membrane>Multi-pass membrane protein.

Extracellular region or secreted Cytosol Plasma membrane Cytoskeleton Lysosome Endosome Peroxisome ER Golgi apparatus Nucleus Mitochondrion Manual annotation Automatic computational assertionSubcellular location
Tissue Specificity:

Widely expressed.

Subunit Structure:

Interacts (via YXXL motif) with MAP1 LC3 family proteins MAP1LC3A, MAP1LC3B and GABARAP.


The YXXL motif mediates the interaction with MAP1 LC3 family proteins MAP1LC3A, MAP1LC3B and GABARAP.

Belongs to the FUN14 family.


1). TBK1 Facilitates GLUT1-Dependent Glucose Consumption by suppressing mTORC1 Signaling in Colorectal Cancer Progression. International Journal of Biological Sciences, 2023 (PubMed: 35637944) [IF=9.2]

2). NTRK1 knockdown induces mouse cognitive impairment and hippocampal neuronal damage through mitophagy suppression via inactivating the AMPK/ULK1/FUNDC1 pathway. Cell death discovery, 2023 (PubMed: 37907480) [IF=7.0]

Application: WB    Species: Mouse    Sample:

Fig. 6 NTRK1 silencing might suppress mitophagy in mouse neurons through the inactivation of the AMPK/ULK1/FUNDC1 pathway. A, B WB revealed that O304 treatment abrogated the suppression effect of NTRK1 knockdown on the activity of the AMPK/ULK1/FUNDC1 pathway in mouse neurons. n = 3. C, D WB also indicated that O304 treatment counteracted the suppression effect of NTRK1 silencing on mitophagy in mouse neurons. n = 3. E, F The results of TOMM20/LC3-II fluorescence staining revealed that the O304 treatment reversed the suppression effect of NTRK1 knockdown on the expression of Parkin in mouse neuronmitochondria. n = 3.

3). Hypoxia‑induced mitophagy regulates proliferation, migration and odontoblastic differentiation of human dental pulp cells through FUN14 domain‑containing 1. International Journal of Molecular Medicine, 2022 (PubMed: 35362539) [IF=5.4]

Application: IHC    Species: Human    Sample: HDPCs

Figure 1 Expressions of inflammatory cytokines, HIF-1α and FUNDC1 in healthy and pulpitis tissues. (A) mRNA expression of IL-1β, IL-6, IL-8 and TNF-α in human healthy and pulpitis tissues. mRNA expression of (B) HIF-1α and (C) FUNDC1 in human healthy and pulpitis tissues. (D) Representative immunostaining images of HIF-1α and FUNDC1 in human healthy or inflamed dental pulp tissues. Scale bars are 100 and 25 µm, respectively. Results are presented as the means ± SD from ≥ three independent experiments. *P<0.05, **P<0.01 and ***P<0.001 vs. healthy. HIF-1α, hypoxia-inducible factor-1α; FUNDC1, FUN14 domain-containing 1.

4). LAMP2A regulates the balance of mesenchymal stem cell adipo-osteogenesis via the Wnt/β-catenin/GSK3β signaling pathway. Journal of Molecular Medicine, 2023 (PubMed: 37162558) [IF=4.7]

5). Human umbilical cord-derived mesenchymal stem cells (hUC-MSCs) alleviate excessive autophagy of ovarian granular cells through VEGFA/PI3K/AKT/mTOR pathway in premature ovarian failure rat model. Journal of Ovarian Research, 2023 (PubMed: 37777781) [IF=4.0]

Application: WB    Species: Rat    Sample:

Fig. 2 hUC-MSC improved the ovarian function of POF rats. A The percentage of each stage in the estrus cycle (the asterisk indicates there are significances in that group by comparing to the other two groups). The serum AMH (B), E2 (C), FSH (D), and LH (E) levels. F Ki67 expression in ovarian GCs; scale bar: 100 μm. G The Western blotting images and quantitation of functional protein expression in GCs. H The fertility and litter size.

6). Molybdenum and Cadmium Co-induce Mitochondrial Quality Control Disorder via FUNDC1-Mediated Mitophagy in Sheep Kidney. Frontiers in Veterinary Science, 2022 (PubMed: 35155662) [IF=3.2]

Application: WB    Species: Sheep    Sample: kidney tissue

Figure 6 Effects of Mo and/or Cd on immunofluorescence of LC3, mitophagy-related mRNA and protein expression levels. (A) The mRNA levels of FUNDC1, LC3A, LC3B and PGAM5. (B) The western blot results of FUNDC1, p-FUNDC1 and LC3. (C) The quantification of FUNDC1, p-FUNDC1 (Ser17) and LC3II/LC3I protein levels. (D) Immunofluorescence co-location of COX IV and LC3 at day 50. In the images, the nucleus staining is shown in blue, COX IV staining is shown in green, LC3 staining is shown in red, and the signals of colocalization are shown in merged images. (E) Pearson coefficient of the colocalization of COX IV and LC3. Data are expressed as means ± SD (n = 6). “*” indicates significant difference compared to the corresponding control (*P < 0.05, **P < 0.01). “#” indicates statistically significant difference between corresponding groups (#P < 0.05, ##P < 0.01).

7). Moxibustion alleviates chronic heart failure by regulating mitochondrial dynamics and inhibiting autophagy. Experimental and Therapeutic Medicine, 2022 (PubMed: 35493422) [IF=2.7]

Application: WB    Species: Rat    Sample:

Figure 6 The effects of MOX on FUNDC1 pathway. (A) The expression levels of ULK1, PGAM5, FUNDC1, p-FUNDC1 and GAPDH. (B) ULK1 relative to GAPDH, (C) PGAM5 relative to GAPDH, (D) FUNDC1 relative to GAPDH. (E) p-FUNDC1 relative to GAPDH. (F) ULK mRNA levels. (G) PGAM5 mRNA levels. (H) FUNDC1 mRNA levels. **P<0.05 vs. C group and #P<0.05 vs. DOX group. Protein levels were measured by western blotting. ULK1, PGAM5 and FUNDC1 mRNA levels were measured by RT-qPCR. Data are mean ± standard deviation from five independent experiments (n=13-20). MOX moxibustion; FUNDC1, FUN14 domain-containing protein 1; ULK1, Unc-51 Like Autophagy Activating Kinase 1; PGAM5, phosphoglycerate mutase family member 5; p-, phosphorylated; DOX, doxorubicin; BEN, benazepril C, control.

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Affinity Biosciences tests all products strictly. Citations are provided as a resource for additional applications that have not been validated by Affinity Biosciences. Please choose the appropriate format for each application and consult Materials and Methods sections for additional details about the use of any product in these publications.

For Research Use Only.
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