// GENETIC INTELLIGENCE PLATFORM

DECODE
THE
CODE
OF LIFE

READY TO PLAY GOD

Reednetics brings precision genomic analysis to researchers and clinicians — turning raw sequence data into clear, actionable intelligence.

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// ANATOMY OF DNA
A — T G — C T — A C — G A — T MAJOR GROOVE MINOR 5' BACKBONE 3' BACKBONE 3.4Å 10 BASE PAIRS / TURN 34Å FULL PITCH
Sugar-Phosphate Backbone (5'→3') Deoxyribose + phosphate linking each nucleotide
Complementary Backbone (3'→5') Antiparallel orientation is essential for replication
A–T Base Pair Adenine–Thymine · 2 hydrogen bonds
G–C Base Pair Guanine–Cytosine · 3 hydrogen bonds (stronger)
WHOLE GENOME SEQUENCING // VARIANT CALLING // EPIGENOMICS // RNA ANALYSIS // POPULATION GENETICS // CRISPR MAPPING // PHARMACOGENOMICS // PROTEOMICS // WHOLE GENOME SEQUENCING // VARIANT CALLING // EPIGENOMICS // RNA ANALYSIS // POPULATION GENETICS // CRISPR MAPPING // PHARMACOGENOMICS // PROTEOMICS //

// THE CENTRAL DOGMA

From molecule
to meaning

Every physical trait, every inherited condition, every biological tendency begins as a sequence of four chemical letters wound into a double helix. Reednetics reads that sequence and translates it into knowledge.

01 // MOLECULE
DNA

Deoxyribonucleic acid — a double-stranded helix made of nucleotide base pairs encoding all genetic information in every cell of the body.

A—T G—C T—A C—G
3.2 billion base pairs per human genome
23 chromosome pairs in every somatic cell
99.9% identical across all humans — variation in 0.1% defines individuality
Reednetics sequences at 30× coverage minimum for clinical accuracy
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02 // SEQUENCE
Gene

A gene is a discrete segment of DNA that encodes instructions for a functional molecule — usually a protein. The human genome contains approximately 20,000 protein-coding genes.

Genes are transcribed to mRNA, then translated to protein
Variants (SNPs, indels, CNVs) within a gene can alter protein function
Pathogenic variants may cause disease; benign variants drive normal diversity
Reednetics classifies variants using ACMG/AMP guidelines
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03 // EXPRESSION
Trait

A trait is any observable characteristic shaped by one or more genes interacting with environment. Traits range from eye color to complex polygenic conditions like kidney disease.

Monogenic traits arise from a single gene (e.g. FSGS, sickle cell)
Polygenic traits involve hundreds of loci acting in concert
Penetrance and expressivity determine how a variant manifests clinically
Reednetics reports penetrance estimates alongside each finding
3.2B
// BASE PAIRS PER GENOME
~20K
// PROTEIN-CODING GENES
99.9%
// SEQUENCING ACCURACY

// GENETIC CONDITIONS

When the code
breaks

Pathogenic variants in specific genes are directly causative of serious heritable conditions. Understanding the genetic architecture of disease is the first step toward precision medicine.

Focal Segmental Glomerulosclerosis
NPHS1 · NPHS2 · WT1 · TRPC6

Scarring of the kidney's filtering units (glomeruli), leading to proteinuria and progressive kidney failure. A leading cause of nephrotic syndrome. Genetic forms are often steroid-resistant.

SEE FULL SPOTLIGHT BELOW
Hypertrophic Cardiomyopathy
MYH7 · MYBPC3 · TNNT2

Abnormal thickening of the heart muscle caused by sarcomere gene variants. The most common inherited cardiac condition — present in 1 in 500 individuals. Leading cause of sudden cardiac death in young athletes.

AUTOSOMAL DOMINANT
BRCA1/2 Breast & Ovarian Cancer
BRCA1 · BRCA2

Pathogenic BRCA1/2 variants dramatically elevate lifetime risk of breast (up to 72%) and ovarian cancer (up to 44%). Hereditary in nature, enabling cascade testing across families for risk stratification.

AUTOSOMAL DOMINANT
Cystic Fibrosis
CFTR

Dysfunction of the CFTR chloride channel causes accumulation of thick mucus in the lungs, pancreas, and digestive tract. Over 2,000 CFTR variants identified; clinical severity varies by variant class.

AUTOSOMAL RECESSIVE
Familial Hypercholesterolemia
LDLR · APOB · PCSK9

Severely elevated LDL cholesterol from birth due to impaired receptor-mediated clearance. Affects 1 in 250; most remain undiagnosed until a cardiovascular event. Early identification enables preventive therapy.

AUTOSOMAL DOMINANT
Marfan Syndrome
FBN1

FBN1 variants cause defective fibrillin-1 in connective tissue, resulting in aortic aneurysm, lens dislocation, and skeletal abnormalities. Life-threatening aortic dissection is the primary risk.

AUTOSOMAL DOMINANT

// CONDITION SPOTLIGHT

Focal Segmental
Glomerulosclerosis

FSGS is not one disease — it is a histological pattern with multiple genetic causes. Identifying the causative variant changes prognosis, treatment, and transplant counseling. Reednetics provides comprehensive FSGS panel testing covering all known pathogenic genes.

1 in 40K
Estimated prevalence
40%
Progress to ESRD within 10 years
30%
Of pediatric FSGS is genetic
~50
Causative genes identified
GLOMERULUS FOCAL SCLEROSIS Healthy capillary loops Sclerotic (scarred) segments Bowman's capsule REEDNETICS PANEL Tests all ~50 FSGS-associated genes in a single assay

// KNOWN CAUSATIVE GENES

Gene Protein Inheritance Notes
NPHS2 Podocin AR Most common genetic cause; steroid-resistant
NPHS1 Nephrin AR Congenital nephrotic syndrome of Finnish type
WT1 Wilms tumor protein AD Associated with Denys-Drash & Frasier syndromes
TRPC6 TRPC6 channel AD Late-onset adult FSGS; gain-of-function
INF2 Inverted formin-2 AD Most common AD form; often with Charcot-Marie-Tooth
COQ2/COQ8B Coenzyme Q pathway AR Mitochondrial FSGS; may respond to CoQ10

// CLINICAL PROGRESSION

STAGE 01
Proteinuria detected

Excessive protein in urine (>3.5g/day = nephrotic range) is often the first sign. Podocyte injury disrupts the glomerular filtration barrier.

STAGE 02
Nephrotic syndrome

Edema, hypoalbuminemia, hyperlipidemia develop. Initial treatment with steroids reveals steroid-resistance in most genetic forms — a key diagnostic clue pointing to underlying mutation.

STAGE 03
Genetic testing

Reednetics FSGS panel identifies the causative variant, classifies inheritance pattern, guides use of calcineurin inhibitors or CoQ10 supplementation (in mitochondrial FSGS), and informs transplant planning.

STAGE 04
Progressive GFR decline

Without effective treatment, glomerular filtration rate falls progressively. Rate of decline varies by gene: NPHS2 variants typically progress faster than INF2-associated disease in adults.

STAGE 05
ESRD & transplant considerations

End-stage renal disease requiring dialysis or transplantation. Critically, genetic FSGS recurrence post-transplant risk depends on the causative gene — NPHS2 low risk, immune-mediated high risk. Genetic diagnosis changes the transplant decision entirely.

// WHY GENETIC DIAGNOSIS MATTERS IN FSGS

Avoids unnecessary immunosuppression in genetic cases (steroid-resistant by definition)
Identifies CoQ10-treatable mitochondrial variants (COQ2, COQ8B, ADCK4)
Predicts post-transplant recurrence risk — changes donor selection and immunosuppression protocol
Enables cascade testing — identifies at-risk family members before clinical presentation
Provides reproductive counseling for families planning future pregnancies
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