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START HERE — how to read ATP + CDK-Tyr15-OH → ADP + CDK-Tyr15-P
A single brake-on cartoon on the human Wee1 kinase-domain frame that exists: 1X8B (1.81 Å), chain A, with inhibitor PD0407824 and Mg. That inhibitor is a named occupancy, not ATP and not the CDK-Tyr15 peptide. ATP and the Tyr15 peptide are [schematic]. Phospho-peptide and ADP are [schematic]. Asp426 is the HMD proton acceptor (UniProt P30291 Active site 426 · proton acceptor). Gold H⁺ parks on Asp426; blue is the Tyr-OH nucleophile, not a hydride. Overlay peptide distances are not geomClaims. PKMYT1 (Myt1, Thr14) is another gene. 2IN6 / 5VCx are not this mesh.
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Crystal structures
PDB 1X8B — human Wee1 kinase domain + PD0407824 + Mg, 1.81 Å (Squire 2005). Coordinates are public. 2IN6 and the 5VCx drug series are more inhibitors — not this mesh. PKMYT1 structures are another gene.
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Mechanism — Asp426 base, in-line γ-PO₃ onto Tyr15-OH
Squire et al., Structure 2005, PMID:15837193 — Wee1A kinase domain with PD0407824. UniProt P30291 annotates residue 426 (the HMD proton acceptor) as Active site; Asp426 is the kinase HMD analog of the HRD base. Lys328 orients ATP. Product is CDK-Tyr15-P, the inhibitory phosphate (brake on). Physiological acceptor teaching = CDK1/2 Tyr15 — analog, not this mesh. Source: Squire 2005 · UniProt P30291
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0 — Setup: PD0407824 occupies the ATP cleft
1X8B holds Wee1, PD0407824, and Mg. The inhibitor is the crystal occupant — not ATP and not the peptide. Opaque, no autoplay. Chemistry below uses schematic ATP + Tyr peptide.Source: PDB 1X8B
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① — CDK-Tyr15 analog presented
A short CDK-Tyr15 analog docks as a named stand-in for CDK1/2 Tyr15 — [schematic], not CDK1 and not a crystal peptide. Tyr OH faces the ATP site. Overlay peptide Å are not geomClaims. Brake teaching = Tyr15, not Thr14.Source: compiled Wee1 substrate identity · UniProt P30291
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② — Schematic ATP docks
Schematic ATP docks into the cleft that crystal PD0407824 occupied — ATP is [schematic], not the inhibitor relabeled. Crystal Mg stays. Asp463 OD1 ⋯ MG = 2.28 Å on this deposit. Overlay ATP / peptide distances are not geomClaims.Source: 1X8B MG pose · schematic ATP
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③ — Asp426 deprotonates the Tyr-OH
(hypothetical, lit.-based) A gold H⁺ sphere rides a gold arrow from peptide OH to Asp426 OD2 and parks. Compiled kinase writes this proton transfer with the γ-PO₃ transfer; this page splits them. Asp426 is not a UniProt ACT_SITE.Source: compiled HMD analog · UniProt P30291
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④ — In-line γ-PO₃ transfer → phospho-Tyr15
(hypothetical, lit.-based) Blue nucleophile rides from peptide OH to ATP PG. Peptide + ATP fade in place to schematic phospho-Tyr15 and schematic ADP. Parked gold H⁺ stays on Asp426. Overlay phospho-peptide Å are not geomClaims. Slow-motion on purpose. Brake on. No covalent phospho-enzyme.Source: compiled Wee1 kinase · UniProt P30291
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⑤ — Products leave — brake on
[schematic] Phospho-Tyr15 and ADP·Mg depart in opposite directions. Parked gold H⁺ leaves toward solvent. Product is the inhibitory CDK-Tyr15-P. PKMYT1 (Thr14) is another gene.Source: EC 2.7.10.2 net accounting
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How to read this page — a first-pass primer
First pass: Setup (PD0407824 seated, Asp426 ★) → ① Tyr15 analog docks → ② schematic ATP docks, Mg stays → ③ gold H⁺ OH → Asp426 (parks) → ④ blue nucleophile OH → PG, peptide+ATP become phospho-Tyr15+ADP → ⑤ products leave; brake on. Second pass: 2.72 / 2.77 / 2.28 Å are crystal facts on 1X8B; ATP, peptide, phospho-peptide, ADP, and the H spheres are [schematic]. Third pass: open “Disagreements” for inhibitor ≠ ATP, analog vs CDK1, PKMYT1, and concerted vs split.
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Chemistry primer — Tyr kinase brake, not CDK2 G1/S
Wee1 transfers ATP γ-phosphate onto CDK Tyr15. Asp426 deprotonates the phenol; the oxygen attacks γ-P in line; ADP leaves. Gold = H⁺. Blue = nucleophile (not hydride). Product is the inhibitory phosphate — brake on. This is not CDK2 phosphorylation of Rb, and not PKMYT1 phosphorylation of Thr14.
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Words used on screen — inhibitor occupancy · analog · brake · PKMYT1
Inhibitor occupancy — PD0407824 is the crystal ligand; never relabeled as ATP. Analog — the Tyr15 peptide is a short model occupancy for CDK1/2 Tyr15. Brake on — CDK-Tyr15-P prevents CDK activation until CDC25 removes it. PKMYT1 — Myt1, Thr14 kinase, another gene. PDB numbering = UniProt P30291 291–575.
Legend & Fidelity
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Mechanism fidelity — measured vs. inferred
The measured layer: 1X8B (1.81 Å) with PD0407824 and Mg; Glu377 O ⋯ INH N1 = 2.72 Å; Cys379 N ⋯ INH O1 = 2.77 Å; Asp463 OD1 ⋯ MG = 2.28 Å. The inferred layer ([schematic]): ATP, Tyr15 peptide, phospho-peptide, ADP, transferring H⁺/nucleophile spheres, product leave, and ③/④ split. Binding order is compiled staging, not a kinetic fit. The protein mesh is static. Overlay peptide contacts are not geomClaims. Asp426 is compiled, not UniProt ACT_SITE.
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Disagreements on record
(a) Inhibitor ≠ ATP ≠ peptide. PD0407824 is occupancy. (b) Peptide ≠ CDK1. Tyr15 analog is a model occupancy. (c) Asp426 is the base. UniProt P30291 Active site 426 (proton acceptor). (d) Concerted vs split. Compiled kinase writes deprotonation + γ-PO₃ transfer as one event; this page splits them (③ then ④). (e) PKMYT1 is another gene (Thr14). (f) 2IN6 / 5VCx are not this mesh. (g) No protein-domain swing.
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Regulation — brake on · CDC25 · PKMYT1 · isoforms
Brake on — Wee1 phosphorylation of CDK-Tyr15 holds CDK inactive. CDC25 removes that phosphate on another page. PKMYT1 (Myt1) phosphorylates Thr14 — other gene, not this mesh. Nuclear teaching isoform. Wee2 is another gene.Source: UniProt P30291 · Squire 2005 PMID:15837193
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Kinetics scope (no measured timecourse on this page)
One ATP + CDK-Tyr15-OH → ADP + CDK-Tyr15-P event is drawn, not a steady-state run. Compiled BRENDA values for EC 2.7.10.2 are not re-asserted here — no measured kcat/Km on this page [schematic]. Pair with a kinetics chapter.Source: BRENDA EC 2.7.10.2 — no kcat/Km re-asserted
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Sequence
Human Wee1 UniProt P30291 · NCBI Gene 7465. Screen uses 1X8B PDB-author numbering = UniProt 291–575. Kinase domain only.
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Simulation map — what you see is what is written
Setup = 1X8B PD0407824 seated (opaque, no autoplay). ① Tyr15 analog moves in (schematic). ② schematic ATP moves in; crystal Mg stays. ③ gold H⁺ + gold arrow OH → Asp426 OD2 (parks). ④ slow-mo: blue nucleophile + blue arrow OH → PG; peptide+ATP fade to phospho-Tyr15+ADP; parked gold H⁺ remains. ⑤ products leave opposite ways; brake on. Only these events move.
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Sources — bibliography of this page
S1 — PDB 1X8B: human Wee1 kinase domain·PD0407824·Mg, 1.81 Å — public coordinates; measured O⋯N1 = 2.72 Å · N⋯O1 = 2.77 Å · OD1⋯MG = 2.28 Å
S2 — Squire et al., Structure 2005, PMID:15837193 — structure and inhibition of human Wee1A
S3 — Sequence: UniProt P30291 (human Wee1) · NCBI Gene 7465
S4 — Kinetics: BRENDA EC 2.7.10.2 — no kcat/Km re-asserted on this page
› Backbones and ligand poses are taken directly from the listed PDB entries,
superposed into one common frame. Where no crystalline state exists for a step
(e.g., ATP identity, Tyr15 peptide, phospho-peptide, ADP after γ-transfer, H⁺ flight, product release), the pose is drawn
schematically and labeled as such in the narration.