Target Atlas
Profiles for the Dark Genome
A growing, open library of computational profiles for proteins the field has left dark — no solved structure, no known ligand, thin literature. Each resolves a sequence into a topology or fold, a disorder map, modification sites, and a predicted pocket, with a validation plan.
Have a dark or under-characterised target? Nominate it — membrane or soluble.
GPR160
Q9UJ42 · 338 aa · PDB: none
The dark oncology / pain orphan with a high-priority pocket hypothesis. No solved structure, no confirmed ligand, contested CARTp biology — resolved into a topology, a residue-level orthosteric-pocket hypothesis, and a validation plan.
GPR149
Q86SP6 · 731 aa · PDB: none
The oversized, disorder-dominated orphan where construct design is the product — an unusually large (731-aa), ~65%-disordered orphan GPCR mapped into truncation boundaries, a pocket hypothesis, and a validation plan.
GPR85
P60893 · 370 aa · PDB: none
The most conserved vertebrate GPCR, still an orphan — a medium-confidence, lipid-adjacent pocket (not forced into a high-confidence claim), with topology, PTM and validation guidance.
GPR27
Q9NS67 · 375 aa · PDB: none
A brain-enriched SREB orphan, highly conserved across vertebrates yet still without a confirmed ligand or a defined function. No solved structure, no confirmed endogenous ligand, only β-cell and metabolic hints — resolved into a topology, a residue-level orthosteric-pocket hypothesis, and a validation plan.
GPR173
Q9NS66 · 373 aa · PDB: none
A reproductive-axis orphan with a named peptide but no solved structure. Phoenixin is reported to signal through GPR173 to activate GnRH and kisspeptin neurons, yet there is no experimental structure and no confirmed small-molecule ligand — resolved into a topology, a residue-level lipid-facing-surface hypothesis, and a validation plan.
GPR176
Q14439 · 515 aa · PDB: none
An orphan that helps set the pace of the circadian clock — Gz-coupled, repressing cAMP with agonist-independent basal activity, and lately tied to cancer progression too. No solved structure, no confirmed ligand — resolved into a topology, a residue-level binding-pocket hypothesis, and a validation plan.
SLC38A11
Q08AI6 · 406 aa · PDB: none
The "putative" SLC38 member, deorphaned in silico — a dark, structureless multi-pass transporter where Astra confirms the transporter identity (p = 1.00) and predicts the substrate-binding cavity.
MFSD8
Q8NHS3 · 518 aa · PDB: none
The lysosomal transporter mutated in CLN7 Batten disease, still structurally dark. No solved structure, an MFS fold inferred from sequence, and a physiological substrate that remains debated — resolved into a twelve-helix topology, a residue-level substrate-cavity hypothesis, post-translational features and a construct plan, computed with Orbion's Astra suite from the sequence alone.
SLC35F2
Q8IXU6 · 374 aa · PDB: none
SLC35F2 is the high-affinity importer of the micronutrient queuine and, incidentally, of the anticancer agent YM155 — over-expressed in non-small-cell lung cancer, yet structurally dark. No solved structure, an SLC35-like fold inferred from sequence — resolved into a ten-helix topology, a residue-level substrate-cavity hypothesis, post-translational features and a construct plan, computed with Orbion's Astra suite from the sequence alone.
SLC22A15
Q8IZD6 · 547 aa · PDB: none
SLC22A15 (FLIPT1) is one of the darkest members of the SLC22 organic-ion transporter family — IDG Tdark, no experimental structure, no established physiological role, and only low-affinity, tentative substrates. There is almost nothing to look up. We resolve the canonical 547-residue sequence into a twelve-helix topology, a residue-level substrate-cavity hypothesis, post-translational features and a construct plan, computed with Orbion's Astra suite from the sequence alone.
TMC7
Q7Z402 · 723 aa · PDB: none
The PIEZO2-tuning channel no one has solved — a structureless multi-pass TMC-family protein where Astra confirms the topology and predicts the pore-lining cavity, for a channel that sets the gain on touch and mechanical pain.
TMEM38B
Q9NVV0 · 291 aa · PDB: none
The dark bone-disease orphan, resolved from sequence alone. TRIC-B is an endoplasmic-reticulum potassium counter-ion channel whose loss disrupts intracellular calcium release and, through it, collagen synthesis — the reported cause of a recessive form of osteogenesis imperfecta. No experimental structure and only a thin functional literature — resolved here into a seven-helix topology, a residue-level allosteric-pocket hypothesis, post-translational features and a construct / validation plan, all computed with Orbion's Astra suite from the canonical 291-residue sequence.
ANO5
Q75V66 · 913 aa · PDB: none
ANO5 (TMEM16E) belongs to the anoctamin family, but unlike its channel relatives it is reported to act in plasma-membrane repair and lipid scrambling rather than as a chloride channel. Recessive loss-of-function mutations cause limb-girdle muscular dystrophy (LGMD2L / LGMDR12) and Miyoshi myopathy, while a dominant gain-of-function variant causes gnathodiaphyseal dysplasia — yet it has no experimental structure in the PDB and a thin functional literature. We resolve the canonical 913-residue sequence into an eight-helix topology, a residue-level pore / interface hypothesis, post-translational features and a construct / validation plan, all computed with Orbion's Astra suite from sequence alone.
ADPRM
Q3LIE5 · 342 aa · PDB: none
A confirmed enzyme with an unsolved human active site — a soluble Mn-dependent hydrolase where Astra confirms the enzyme class and predicts a di-metal active-site pocket that lands on its catalytic residues.
MDH1B
Q5I0G3 · 518 aa · PDB: none
A soluble "putative" malate dehydrogenase whose activity has never been shown — Astra confirms it is a real oxidoreductase and flags a high-confidence pocket in its unusual N-terminal extension.
OVCA2
Q8WZ82 · 227 aa · PDB: none
A soluble esterase from an ovarian-cancer deletion locus — Astra recovers its hydrolase identity from sequence and lands the predicted pocket on the Ser–His–Asp catalytic triad, for a protein with no solved structure and no known substrate.
MINDY4
Q4G0A6 · 757 aa · PDB: none
A predicted function, an active-site pocket that lands on the catalytic dyad, and a modification map — for a soluble deubiquitinase with no solved structure and unconfirmed activity.
SCYL3
Q8IZE3 · 742 aa · PDB: none
A predicted function call, a degenerate kinase pocket, and a modification map — for a soluble pseudokinase with no solved structure and no known substrate.
ABHD17A
Q96GS6 · 310 aa · PDB: none
ABHD17A is a serine hydrolase that strips palmitate from S-acylated proteins — among them N-Ras, whose membrane localisation and oncogenic signalling depend on an intact palmitoylation cycle. Yet it remains an IDG Tbio enzyme with no experimental structure in the PDB and a thin literature. We resolve the canonical 310-residue sequence into its α/β-hydrolase fold, a residue-level active-site hypothesis clustered around the catalytic triad, post-translational features and a construct / validation plan — all computed with Orbion's Astra suite from sequence alone.
METTL7B
Q6UX53 · 244 aa · PDB: none
The dark thiol-methyltransferase sitting between xenobiotic metabolism and cancer biology. METTL7B has no solved structure, no named ligand, and a scattered literature — yet it is reported to methylate small-molecule thiols such as hydrogen sulfide and the drug captopril, and to be required for tumour-cell proliferation. We resolve the canonical 244-residue sequence into a membrane topology, a residue-level active-site hypothesis, and a construct / validation plan, computed with Orbion's Astra suite from sequence alone.
NAT8
Q9UHE5 · 227 aa · PDB: none
The dark ER-membrane acetyltransferase behind one of the more reproducible kidney-function GWAS signals. NAT8 has no solved structure and a thin functional literature, yet it catalyses the final step of mercapturic-acid detoxification and N6-lysine acetylation inside the endoplasmic reticulum — and its variants track with kidney function and N-acetylated metabolite levels. We resolve the canonical 227-residue sequence into a type II membrane topology, a residue-level active-site hypothesis, and a construct / validation plan, computed with Orbion's Astra suite from sequence alone.
SCYL1
Q96KG9 · 808 aa · PDB: none
A catalytically dead kinase look-alike whose loss causes an inherited neurodegeneration syndrome. SCYL1 is a pseudokinase — a kinase-shaped scaffold that has lost its catalytic activity — that helps run COPI-mediated retrograde traffic at the Golgi; recessive loss-of-function causes CALFAN — a childhood syndrome of low-γ-GT cholestasis, acute liver failure and spinocerebellar neurodegeneration. No solved structure, no named ligand. We resolve the canonical 808-residue sequence into a domain map, a residue-level allosteric-pocket hypothesis, disorder boundaries and a validation plan, computed with Orbion's Astra suite from sequence alone — and because it is a pseudokinase, we frame the pocket as an allosteric / regulatory site, not a catalytic one.
FAM111B
Q6SJ93 · 734 aa · PDB: none
The rare-disease enzyme with a predicted catalytic triad and no crystal to check it against. Dominant FAM111B mutations cause POIKTMP — a multisystem disorder of skin, tendon, muscle and lung — and the same protease has been reported as a p53-driven player in lung adenocarcinoma, yet the PDB is empty. We resolve the canonical 734-residue sequence into a topology, a residue-level active-site hypothesis, post-translational features and a construct / validation plan, computed with Orbion's Astra suite from sequence alone.
TMEM43
Q9BTV4 · 400 aa · PDB: none
LUMA — behind a lethal cardiomyopathy and two more Mendelian diseases; a structureless inner-nuclear-membrane protein resolved into a topology, a disease-variant structural map, and a predicted pocket.
CLPTM1L
Q96KA5 · 538 aa · PDB: none
A membrane protein famous for its address, not its mechanism. CLPTM1L sits beside TERT at 5p15.33 — one of the most repeatedly cancer-associated loci in the genome — yet its day job, scrambling GPI-precursor lipids across the ER membrane, has no solved structure to reason over. We resolve the canonical 538-residue sequence into a six-helix topology, a residue-level membrane-facing pocket hypothesis, post-translational features and a construct / validation plan, computed with Orbion's Astra suite from sequence alone.
ABI3
Q9P2A4 · 366 aa · PDB: none
A top-tier Alzheimer's genetic hit whose mechanism is unknown — a structureless, half-disordered adaptor resolved into a domain map, a construct-design plan, and an interaction pocket on its SH3 domain.
FAM222A
Q5U5X8 · 452 aa · PDB: none
"Aggregatin" — an Aβ-nucleating protein with no structure that AlphaFold resolves poorly; Astra maps its order/disorder and flags a tractable, high-confidence pocket distinct from its Aβ-binding region.
SAMD9L
Q8IVG5 · 1,584 aa · PDB: none
Three inherited diseases, one structureless giant — a huge multidomain effector behind ataxia-pancytopenia, monosomy-7 myelodysplasia and SCA49; Astra maps its architecture, places disease variants in context, and predicts an effector-core pocket.
WDR89
Q96FK6 · 387 aa · PDB: none
The conserved-but-dark propeller, newly tied to genome maintenance — a predicted seven-bladed β-propeller with no solved structure, resolved into a fold, a protein-interaction pocket, and a validation plan.
FAM171A2
A8MVW0 · 826 aa · PDB: none
One of the darkest proteins with a credible Parkinson's link. FAM171A2 is IDG Tdark — no solved structure, no catalogued molecular function — yet it has been reported to sit on neurons and pull in α-synuclein fibrils, and to act as a genetic regulator of progranulin and neurodegeneration risk. We resolve the canonical 826-residue sequence into a signal-peptide-plus-single-pass topology, a residue-level surface-pocket hypothesis in the ectodomain, a long disordered cytoplasmic tail and a construct / validation plan, computed with Orbion's Astra suite from sequence alone.
Turn a Dark Target Into an Experiment-Ready Plan
Send a UniProt ID and Orbion returns a characterisation preview like the ones above — topology or fold, disorder, PTMs, a pocket or active-site hypothesis, and recommended validation experiments. New targets go up every week.