NDUFV1 Antibody

What is NDUFV1 and why is it significant for mitochondrial research?

NDUFV1 represents the 51-kD subunit of complex I (NADH:ubiquinone oxidoreductase) in the mitochondrial respiratory chain, playing a crucial role in electron transfer from NADH to the respiratory chain . The significance of NDUFV1 extends beyond its structural role, as it contributes to maintaining mitochondrial homeostasis particularly during cellular stress conditions . NDUFV1 mutations have been associated with several mitochondrial disorders including Leigh syndrome, Leigh-like syndrome, diffuse leukoencephalopathy, and neurodegenerative conditions such as Parkinson's disease . Recent findings indicate that NDUFV1 expression levels change in response to pathological conditions like renal ischemia-reperfusion injury, positioning it as a potential therapeutic target for conditions involving mitochondrial dysfunction .

Which applications are NDUFV1 antibodies typically used for?

NDUFV1 antibodies have demonstrated utility across multiple experimental applications, with consistent performance in:

These antibodies have been successfully used to examine NDUFV1 expression changes in various experimental models, including renal ischemia-reperfusion injury and mitochondrial complex I deficiency studies .

How should researchers select appropriate positive and negative controls for NDUFV1 antibody validation?

Proper control selection is critical for ensuring antibody specificity and experimental validity. For NDUFV1 antibody work:

Positive controls:

• 293T cell lysates have been validated as effective positive controls for NDUFV1 detection

• Tissues with high mitochondrial content (heart, kidney, liver) typically express detectable levels of NDUFV1

• Recombinant NDUFV1 protein (particularly fragments corresponding to amino acids 218-459)

Negative controls:

• NDUFV1 knockout cell lines provide the most stringent negative controls, as demonstrated in validated Western blot applications

• NDUFV1 knockdown samples using siRNA approaches (multiple siRNA oligomers should be used to control for off-target effects)

• Tissues from species outside the antibody's known cross-reactivity profile

The inclusion of both control types significantly enhances result interpretation validity and antibody specificity confirmation .

What is the cross-species reactivity profile of commonly available NDUFV1 antibodies?

Most commercial NDUFV1 antibodies demonstrate a broad cross-reactivity profile due to the high sequence conservation of NDUFV1 across species. The typical reactivity profile includes:

This extensive cross-reactivity stems from the conserved peptide sequence (FMNKPSDGRP KYLVVNADEG EPGTCKDREI LRHDPHKLLE GCLVGGRAMG) targeted by many NDUFV1 antibodies . When working with non-validated species, preliminary validation experiments are strongly recommended.

What are the optimal storage and handling conditions for NDUFV1 antibodies?

Proper storage and handling significantly impact antibody performance and longevity:

• Store concentrated antibody solutions at -20°C for long-term storage

• For frequent use, small aliquots at 4°C remain stable for approximately 2-4 weeks

• Avoid repeated freeze-thaw cycles which can degrade antibody quality

• Most NDUFV1 antibodies are supplied in PBS with 20% glycerol and 0.025% ProClin 300 at pH 7.0

• Always centrifuge briefly before opening the vial to collect any solution that may be trapped in the cap

• Working dilutions should be prepared fresh and used within 24 hours

• For antibodies with carrier proteins, ensure compatibility with your detection system

Research indicates that antibody stability is optimized when stored in their original buffer conditions rather than after dilution in working solutions .

How can NDUFV1 antibodies be used to investigate mitochondrial complex I deficiency models?

NDUFV1 antibodies serve as valuable tools for investigating mitochondrial complex I deficiency models through several sophisticated approaches:

Experimental approach protocols:

• Knockdown validation studies:

  • NDUFV1 siRNA experiments require antibody-based confirmation of knockdown efficiency

  • Multiple siRNA oligomers should be used to control for off-target effects

  • Western blot analysis using NDUFV1 antibodies at 1:1000 dilution consistently shows knockdown efficiency between 70-90%

• Functional impact assessment:

  • NDUFV1 knockdown leads to complex I dysfunction, enhancing rather than preventing skeletal myogenesis

  • This can be quantified by increased nuclei number in MyHC-positive cells (~4-fold increase in 3-day differentiated myotubes)

  • NDUFV1 antibodies help verify that observed phenotypes are specifically related to NDUFV1 deficiency

• Metabolic consequence analysis:

  • NDUFV1 deficiency affects the NAD⁺/NADH ratio, influencing SIRT1 activity

  • Glycolysis activation as compensatory mechanism can be correlated with NDUFV1 protein levels

  • Interestingly, ATP levels remain unchanged despite complex I dysfunction due to upregulated glycolysis

These studies highlight how NDUFV1 antibodies enable mechanistic insights into complex I deficiency beyond simple protein detection.

What methodological approaches can optimize NDUFV1 detection in tissue samples with variable expression levels?

Detecting NDUFV1 in tissues with variable expression presents specific challenges requiring methodological optimization:

For immunohistochemistry optimization:

• Antigen retrieval protocol selection:

  • Heat-induced epitope retrieval (HIER) using citrate buffer (pH 6.0) for 20 minutes at 95°C yields optimal results for most NDUFV1 epitopes

  • For difficult samples, test alternative retrieval buffers (EDTA pH 8.0 or Tris-EDTA pH 9.0)

• Signal amplification options:

  • Tyramide signal amplification (TSA) can enhance sensitivity by 10-100 fold for low-expressing tissues

  • Polymer-based detection systems generally provide superior results compared to ABC methods

• Blocking optimization:

  • Extended blocking (2 hours) with 5% non-fat milk in PBS significantly reduces background in renal tissues

  • Include 0.1% Triton X-100 in blocking solution for improved antibody penetration

• Exposure time considerations:

  • Extended primary antibody incubation (overnight at 4°C) improves detection of low abundance NDUFV1

  • Titration experiments with dilution series (1:50 to 1:500) should be performed for each new tissue type

For renal tissue specifically, studies have shown optimal NDUFV1 detection using overnight incubation at 4°C with 1:200 antibody dilution following citrate buffer antigen retrieval .

How can researchers effectively use NDUFV1 antibodies to study mitochondrial dynamics in acute kidney injury models?

NDUFV1 antibodies serve as valuable tools for investigating mitochondrial involvement in acute kidney injury (AKI) models:

Methodological workflow:

• Model establishment and validation:

  • Renal ischemia/reperfusion (I/R) injury in C57BL/6 mice decreases NDUFV1 expression by approximately 60%

  • Verification requires careful timing with NDUFV1 antibody assessment at 36 hours post-I/R surgery

• Therapeutic intervention assessment:

  • In vivo NDUFV1 overexpression via plasmid delivery (10 μg via tail vein injection) can be monitored using antibody-based techniques

  • This approach shows successful restoration of NDUFV1 protein levels, even exceeding those in sham controls

• Multi-parameter mitochondrial assessment:

  • NDUFV1 antibodies can be used alongside other mitochondrial markers (SDHA, HSP60, PHB1, VDHC, Cox IV) for comprehensive mitochondrial evaluation

  • This combination allows correlation between NDUFV1 levels and apoptotic markers (Bax, Bcl-2, cleaved Caspase-3)

• Quantification approaches:

  • Western blot analysis with NDUFV1 antibodies shows that successful overexpression increases renal NDUFV1 levels by approximately 2.5-fold compared to sham controls

  • This correlates with significantly reduced BUN and serum creatinine levels (approximately 65% reduction)

This approach has successfully demonstrated that NDUFV1 reinforcement protects against renal I/R injury by improving mitochondrial function and reducing oxidative stress .

What are the methodological considerations for using NDUFV1 antibodies in studying the relationship between complex I function and cellular metabolism?

When investigating complex I function and metabolism using NDUFV1 antibodies, several methodological considerations enhance experimental rigor:

Integrated experimental approach:

• Coordinated protein and activity measurements:

  • NDUFV1 protein detection should be paired with complex I activity assays

  • Protein levels often don't directly correlate with enzymatic activity, necessitating both measurements

• Metabolic profiling integration:

  • NDUFV1 knockdown studies reveal that despite complex I dysfunction, ATP levels may remain unchanged due to compensatory glycolysis

  • Measurement protocol should include:

    • NDUFV1 protein quantification (Western blot)

    • ATP content measurement (luminescence-based assays)

    • Glycolysis assessment (pyruvate/lactate measurements)

    • NAD⁺/NADH ratio determination

• Timeline considerations:

  • Acute vs. chronic NDUFV1 deficiency produces different metabolic adaptations

  • Experimental designs should include multiple timepoints (24h, 48h, 72h) for knockdown studies

• Subcellular localization assessment:

  • NDUFV1 antibodies can be used for mitochondrial fraction confirmation

  • Differential centrifugation protocols combined with Western blotting provide subcellular resolution

This integrated approach has revealed that NDUFV1 deficiency-induced complex I dysfunction alters NAD⁺/NADH ratios, influencing SIRT1 activity and consequently enhancing skeletal myogenesis .

How can dual antibody approaches reveal NDUFV1's interactions with other mitochondrial proteins?

Using multiple antibodies simultaneously can provide deeper insights into NDUFV1's functional relationships with other mitochondrial components:

Dual antibody methodological approaches:

• Co-immunoprecipitation protocols:

  • NDUFV1 antibodies can be used for protein complex pulldown followed by detection of interacting partners

  • Recommended lysis conditions: RIPA buffer with protease inhibitors and 1 mM PMSF

  • Gentle elution (non-denaturing) preserves protein-protein interactions

• Proximity ligation assay (PLA):

  • Combines two primary antibodies (NDUFV1 and potential interactor)

  • Secondary antibodies with attached DNA probes generate fluorescent signal only when proteins are within 40 nm

  • Particularly valuable for detecting transient interactions in intact cells

• Sequential immunoblotting:

  • Western blots can be stripped and reprobed to detect multiple proteins

  • For NDUFV1 research, successful sequential detection has been demonstrated with:

    • NDUFV1 (51 kDa)

    • SDHA (70 kDa)

    • HSP60 (60 kDa)

    • PHB1 (30 kDa)

    • VDHC (32 kDa)

    • Cox IV (17 kDa)

• Multiplex immunofluorescence:

  • Carefully selected primary antibodies from different host species

  • Species-specific secondary antibodies with distinct fluorophores

  • Avoids cross-reactivity while enabling simultaneous visualization

These methodologies have revealed important functional relationships between NDUFV1 and other mitochondrial proteins in the context of kidney injury and metabolic regulation .

What are the most common issues encountered when using NDUFV1 antibodies and their solutions?

Researchers frequently encounter several challenges when working with NDUFV1 antibodies that can be systematically addressed:

When troubleshooting, systematic evaluation of each variable is recommended. For Western blot applications specifically, researchers have found that loading 30 μg of protein extract and using 1:1000 antibody dilution provides optimal results for NDUFV1 detection .

How can researchers validate NDUFV1 antibody specificity for their specific experimental system?

Thorough antibody validation is essential for ensuring experimental rigor and reproducibility:

Comprehensive validation strategy:

• Genetic manipulation approaches:

  • NDUFV1 knockout validation: Wild-type and NDUFV1 knockout 293T cell extracts demonstrate antibody specificity when the signal is present only in wild-type samples

  • NDUFV1 knockdown: Multiple siRNA oligomers targeting different regions of NDUFV1 should produce consistent reduction in signal intensity

  • Overexpression: Plasmid-based NDUFV1 expression should increase signal intensity proportionally

• Peptide competition assays:

  • Pre-incubation of antibody with immunizing peptide (FMNKPSDGRP KYLVVNADEG EPGTCKDREI LRHDPHKLLE GCLVGGRAMG) should abolish specific signal

  • Non-specific peptides should have no effect on signal intensity

  • Titration series with increasing peptide concentrations provides quantitative specificity assessment

• Cross-platform validation:

  • Concordance between detection methods (WB, IHC, IF) increases confidence in specificity

  • Correlation between protein detection and mRNA levels provides additional validation

  • Multiple antibodies targeting different NDUFV1 epitopes should show similar patterns

• Non-immune controls:

  • Isotype control antibodies from the same species identify non-specific binding

  • Secondary-only controls detect potential direct binding to endogenous immunoglobulins

These validation approaches ensure that experimental findings truly reflect NDUFV1 biology rather than antibody artifacts.

What are the optimal sample preparation methods for preserving NDUFV1 epitopes in different experimental contexts?

Sample preparation significantly impacts NDUFV1 antibody performance across different applications:

For Western blotting:

• Optimal lysis buffer: RIPA buffer (25 mM Tris-HCl pH 7.6, 150 mM NaCl, 1% NP-40, 1% sodium deoxycholate, 0.1% SDS) with protease inhibitor cocktail

• Sample denaturation: 5 minutes at 95°C in standard Laemmli buffer with 5% β-mercaptoethanol

• Protein loading: 30 μg total protein consistently produces clear bands at the expected 51 kDa size

• Gel percentage: 10% SDS-PAGE provides optimal resolution for NDUFV1

For immunohistochemistry:

• Fixation: 10% neutral buffered formalin for 24-48 hours

• Processing: Standard paraffin embedding with minimal processing time to prevent epitope loss

• Sectioning: 4-5 μm sections yield optimal results

• Antigen retrieval: Heat-induced epitope retrieval with sodium citrate buffer (pH 6.0) for 20 minutes

For immunofluorescence:

• Fixation: 4% paraformaldehyde (10 minutes at room temperature)

• Permeabilization: 0.1% Triton X-100 in PBS (5 minutes)

• Blocking: 5% BSA or non-fat milk in PBS (1-2 hours)

• Antibody dilution: 1:200-1:500 in blocking buffer

These optimized protocols ensure maximal epitope preservation and accessibility while minimizing non-specific binding.

What technical considerations should be addressed when using NDUFV1 antibodies in multiplex immunofluorescence studies?

Multiplex immunofluorescence with NDUFV1 antibodies requires careful attention to several technical factors:

Comprehensive optimization strategy:

• Antibody compatibility assessment:

  • Primary antibodies must be from different host species (e.g., rabbit anti-NDUFV1 with mouse anti-mitochondrial markers)

  • When using same-species antibodies, sequential detection with directly labeled antibodies prevents cross-reactivity

  • Antibody fragment approaches (Fab fragments) can overcome species limitations

• Signal separation strategies:

  • Spectral unmixing for closely emitting fluorophores

  • Use fluorophores with >50 nm separation between emission peaks

  • For NDUFV1 colocalization with mitochondrial markers, recommended combinations:

    • NDUFV1 (Alexa 488) with Cox IV (Alexa 594)

    • NDUFV1 (Alexa 647) with HSP60 (Alexa 555)

• Optimal fixation for multiple epitopes:

  • Combined approaches may be necessary (e.g., brief PFA fixation followed by methanol)

  • Systematic testing of fixation protocols for each antibody individually before multiplexing

  • For mitochondrial studies, 4% PFA for 10 minutes followed by 0.1% Triton X-100 permeabilization works well for most combinations

• Image acquisition considerations:

  • Sequential scanning to prevent spectral bleed-through

  • Identical acquisition settings between experimental groups

  • Z-stack imaging for complete mitochondrial network analysis

These approaches have successfully enabled simultaneous visualization of NDUFV1 with other mitochondrial proteins in studies of mitochondrial function and dynamics.

How can researchers quantitatively assess NDUFV1 expression changes in disease models using antibody-based approaches?

Quantitative assessment of NDUFV1 expression requires rigorous methodological approaches:

Quantification protocols:

• Western blot densitometry:

  • Loading controls: β-actin provides reliable normalization for whole-cell extracts

  • For mitochondrial fractions, VDAC or Cox IV are preferred normalization controls

  • Technical replicates: Minimum of three independent experiments

  • Software options: ImageJ with background subtraction and ROI-based analysis

  • Validation study showed NDUFV1 expression decreased by approximately 60% in renal I/R model mice

• Immunohistochemistry quantification:

  • Tissue microarray approach for high-throughput analysis

  • Digital pathology algorithms for automated scoring

  • H-score method combining intensity and percentage positive cells:

    • Score = (% weak × 1) + (% moderate × 2) + (% strong × 3)

  • Minimum of 5 representative fields at 20× magnification

• Flow cytometry for NDUFV1:

  • Fixation and permeabilization optimization critical

  • Median fluorescence intensity (MFI) provides reliable quantification

  • Comparison to isotype controls essential

  • Minimum of 10,000 events per sample

• Normalization strategies:

  • For tissue heterogeneity: normalize to cell-type specific markers

  • For sample variability: use multiple housekeeping proteins

  • For inter-experimental variation: include standard sample across experiments

These quantitative approaches have successfully demonstrated that NDUFV1 expression decreases significantly in renal I/R injury but can be effectively restored through genetic intervention strategies .

How are NDUFV1 antibodies being used to investigate the relationship between mitochondrial dysfunction and disease pathogenesis?

NDUFV1 antibodies have become instrumental in elucidating the mechanistic connections between mitochondrial dysfunction and disease development:

Current research applications:

• Renal pathophysiology:

  • NDUFV1 reduction corresponds with kidney dysfunction in ischemia/reperfusion models

  • Antibody-based detection reveals that NDUFV1 reinforcement attenuates proximal tubule injury

  • Decreased BUN and serum creatinine levels correlate with restored NDUFV1 expression

• Neurodegenerative disease connections:

  • NDUFV1 mutations are linked to Leigh syndrome, Leigh-like syndrome, and Parkinson's disease

  • Antibody-based approaches help characterize the molecular consequences of these mutations

  • Studies monitor NDUFV1 protein stability, mitochondrial localization, and complex I integration

• Skeletal muscle metabolism:

  • NDUFV1 knockdown counterintuitively enhances rather than inhibits skeletal myogenesis

  • This enhancement involves a 4-fold increase in nuclei number in MyHC-positive cells

  • The mechanism operates through NAD⁺/NADH ratio changes affecting SIRT1 activity

• Metabolic adaptation assessment:

  • Despite complex I dysfunction from NDUFV1 deficiency, ATP levels remain unchanged

  • Antibody-based measurements coupled with metabolic assays reveal compensatory glycolysis activation

  • Increased pyruvate and lactate production maintain energy homeostasis

These diverse applications demonstrate how NDUFV1 antibodies enable mechanistic insights into disease pathogenesis beyond simple protein detection.

What is the current understanding of the relationship between NDUFV1 and oxidative stress in mitochondrial pathology?

Research using NDUFV1 antibodies has revealed complex relationships between NDUFV1 function and oxidative stress regulation:

Mechanistic insights:

• Protective role in renal injury:

  • NDUFV1 overexpression significantly reduces oxidative stress markers in renal I/R injury models

  • This protection operates through improved mitochondrial integrity and function

  • Decreased cell apoptosis correlates with NDUFV1 expression levels

• Apoptotic regulation mechanisms:

  • NDUFV1 reinforcement alters the expression ratio of pro-apoptotic (Bax) and anti-apoptotic (Bcl-2) proteins

  • Specifically, NDUFV1 prevents the I/R-induced increase in Bax and decrease in Bcl-2

  • This results in a significantly reduced Bax/Bcl-2 ratio, a key determinant of apoptotic susceptibility

• ROS production paradox:

  • Despite NDUFV1's role in complex I, knockdown doesn't always increase reactive oxygen species

  • Studies using DCF-DA staining show no change in ROS production in some NDUFV1-deficient models

  • This suggests context-dependent relationships between complex I dysfunction and oxidative stress

• Mitochondrial membrane potential maintenance:

  • NDUFV1 knockdown in certain cellular contexts doesn't alter membrane potential

  • MitoTracker CMXRos measurements remain unchanged despite complex I dysfunction

  • This indicates efficient compensatory mechanisms for maintaining mitochondrial function

These findings highlight that targeting NDUFV1 and mitochondrial function represents a promising therapeutic approach for diseases characterized by oxidative stress and mitochondrial dysfunction .

How can NDUFV1 antibodies be used in screening potential therapeutic compounds targeting mitochondrial function?

NDUFV1 antibodies provide valuable tools for evaluating therapeutic interventions targeting mitochondrial function:

Screening methodology framework:

• Expression-based primary screening:

  • NDUFV1 antibodies enable high-throughput screening of compounds that modulate its expression

  • In-cell Western or automated immunofluorescence platforms support large-scale screening

  • Quantitative readouts correlate with functional outcomes in disease models

• Functional validation cascade:

  • Primary hits undergo secondary validation using NDUFV1 antibodies to confirm:

    • Protein expression changes (Western blot)

    • Subcellular localization (immunofluorescence)

    • Integration into complex I (co-immunoprecipitation)

  • This multi-parameter assessment narrows candidates to those with desired mechanistic profiles

• Disease model evaluation:

  • Renal I/R injury models have demonstrated that NDUFV1 reinforcement provides multiple benefits:

    • Reduced serum creatinine and BUN levels

    • Attenuated proximal tubule injury

    • Mitigated cell apoptosis

  • These endpoints provide translational relevance for therapeutic development

• Correlation with mitochondrial integrity:

  • Effective compounds should improve mitochondrial markers detectable with antibody panels:

    • Structural proteins: HSP60, PHB1

    • Functional components: SDHA, VDHC, Cox IV

  • Quantitative relationships between these markers and NDUFV1 levels inform mechanism of action

This approach has successfully demonstrated that targeting NDUFV1 and mitochondrial function represents a promising strategy for treating kidney diseases characterized by mitochondrial dysfunction .

What methodological approaches are being developed to study NDUFV1 post-translational modifications using specific antibodies?

Emerging methodologies are enhancing our ability to study NDUFV1 post-translational modifications (PTMs):

Advanced PTM detection approaches:

• Phospho-specific antibody development:

  • Custom antibodies targeting predicted phosphorylation sites on NDUFV1

  • Validation workflow includes:

    • Phosphatase treatment controls

    • Phosphomimetic mutant expression

    • Mass spectrometry correlation

  • This approach can identify regulatory phosphorylation events affecting NDUFV1 function

• Ubiquitination and SUMOylation assessment:

  • Two-step immunoprecipitation protocols:

    • First IP: Ubiquitin/SUMO antibodies

    • Second detection: NDUFV1 antibodies

  • Alternative approach: NDUFV1 immunoprecipitation followed by ubiquitin/SUMO detection

  • These modifications may regulate NDUFV1 stability and turnover

• Acetylation status determination:

  • Given NDUFV1's relationship with NAD⁺/NADH ratio and SIRT1

  • Acetylation status may be a key regulatory mechanism

  • Acetyl-lysine antibodies combined with NDUFV1 immunoprecipitation

  • Mass spectrometry validation of specific acetylation sites

• Redox modification analysis:

  • Redox proteomics approaches with NDUFV1 antibodies

  • Differential alkylation protocols to trap oxidation states

  • May explain oxidative stress responses in pathological conditions

These methodologies promise to reveal how PTMs regulate NDUFV1 function, potentially identifying novel therapeutic targets for mitochondrial dysfunction.

How do different experimental models impact NDUFV1 expression patterns and antibody detection strategies?

Experimental models significantly influence NDUFV1 expression and detection requirements:

Model-specific considerations:

• Cell culture systems:

  • Immortalized cell lines (293T, TCMK-1) show consistent NDUFV1 expression

  • Detection protocol: Standard Western blot with 30 μg protein loading at 1:1000 antibody dilution

  • C2C12 myoblasts exhibit significant expression changes during differentiation

  • Knockdown efficiency reaches 70-90% using siRNA approaches

• Animal models:

  • Renal I/R injury in C57BL/6 mice reduces NDUFV1 expression by approximately 60%

  • Plasmid expression via tail vein injection (10 μg in 8-12s) successfully increases NDUFV1

  • Expression peaks 48 hours post-injection, primarily in renal glomeruli and tubules

  • Tissue-specific expression patterns require optimization of detection protocols

• Human patient samples:

  • Formalin-fixed paraffin-embedded (FFPE) tissues require extended antigen retrieval

  • Fresh frozen tissues yield superior signal with less background

  • Patient heterogeneity necessitates larger sample sizes for meaningful comparisons

• Specialized detection requirements:

  • Zebrafish models: Despite 87% sequence homology, require higher antibody concentrations

  • Xenopus models: 90% sequence homology, validate with morpholino controls

  • Tissue microarrays: Enable high-throughput screening across multiple samples

These model-specific considerations inform optimal experimental design and appropriate antibody selection for investigating NDUFV1 biology in different research contexts.

What are the future directions for NDUFV1 antibody applications in mitochondrial research?

The field of NDUFV1 research continues to evolve with several promising future directions:

• The development of more specific and sensitive antibodies targeting distinct NDUFV1 epitopes and post-translational modifications will enable more nuanced investigations of its regulation and function .

• Integration of NDUFV1 antibody-based detection with advanced imaging techniques like super-resolution microscopy and correlative light and electron microscopy will provide unprecedented insights into mitochondrial complex I dynamics.

• Therapeutic strategies targeting NDUFV1 expression or function show promise for treating conditions characterized by mitochondrial dysfunction, including acute kidney injury and neurodegenerative disorders .

• Combined approaches using NDUFV1 antibodies with metabolic profiling technologies will further elucidate the complex relationships between complex I function, cellular metabolism, and disease pathogenesis .