Hypoxia and nicotine alter endothelial nicotinic-receptor expression. Beta2-specific changes are reported without displayed data; the angiogenesis pharmacology mainly implicates alpha7.

Authentic abstract reports beta2 I312M increases receptor ACh sensitivity. Sensitivity changes alone do not separate binding affinity from gating. Search found request-only author page and limited publisher sections, not full electrophysiology. Underlying beta2 ligand contribution is independently supported by the 2024 ACh structures.

Authentic abstract explicitly includes human alpha6beta2 and alpha6beta2beta3 assemblies, expression/ligand-binding and cell-system differences. Full current assay protocol not independently accessed; beta3 assembly effects are not assigned as a beta2-specific chaperone function.

Authentic abstract explicitly reports human concatemer-defined receptor stoichiometries, M2 charge mutations and calcium permeability differences. Full Methods not recovered here; use the full text of PMID:20881005 for inspected calcium-current methodology.

Human CHRNB2 variants associate with cognitive-task differences in a female student cohort stratified by smoking history. Association does not identify a directly measured nicotine-induced behavioral change.

A human CHRNB2 V287M variant segregates with familial epilepsy; the clinical pedigree does not establish a separate molecular function.

Human receptor clones expressed in Xenopus yielded baseline ACh responses; mouse Pate-P inhibited human alpha4beta2 net charge. Mixed species of modulator and receptor are explicit. PATE modulation is not proof that CHRNB2 itself is a secreted modulator.

Selected abstract centers on CHRNA5 ethanol-responsive expression; it does not resolve the background sentence behind beta2 TAS. Do not call wrong-gene miscitation from that abstract. Actual beta2 channel capability is independently secure; exact TAS linkage remains unverified.

Actual human beta2-alpha4-beta2-alpha4 concatemer plus free alpha5 was tested by voltage clamp and calcium-only currents; the study also tested alpha3beta2alpha5. Full primary resides in preserved CHRNA4 normal/research variant, not the CHRNB2 abstract archive. Alpha5 D398N effect is not transferred to beta2. The reported calcium-only normalization method is retained without claiming an independently calculated permeability coefficient.

Human alpha2 with beta2 produces agonist currents; codon-optimized beta2 improves expression and was used for subsequent assays. Single-subunit negative controls lack functional receptor. Expression ratios bias putative stoichiometries; exact assembly was not directly counted here. The tested disease-associated variant is alpha2 T22I, not a beta2 mutation.

Recombinant human LYPD6 captures beta2-containing receptors from human cortex, with uncoupled-bead and knockout antibody controls. This is complex association, not purified binary affinity.

Human alpha4/beta2 form a heteropentameric pore. Nicotine occupies alpha4(+)/beta2(-) interfaces, with beta2 loopD/E residues contributing. Direct ACh patch-clamp comparison supports both full-length and engineered crystallization constructs. Structure uses intracellular-loop deletions, junction linker and beta2 C-terminal Strep tag; prolonged nicotine produces a desensitized nonconducting structure. Structural state does not negate measured currents.

Both human alpha4beta2 stoichiometries were structurally resolved. The 3alpha:2beta form has an additional alpha-alpha nicotine site; beta2 complementary face and M2 charge composition explain receptor differences. Same large intracellular-loop deletions and tag; calcium-permeability ratio is cited prior physiology, not a new flux measurement in the inspected structural Results.

Tagged human HEK293T AP-MS records alpha5 and beta2 in the same interaction network. The exact spoke-expanded positive pair supports association without defining native receptor stoichiometry.

Human alpha7-beta2 concatemer in Xenopus oocytes supports ACh-evoked currents and conotoxin selectivity. Enforced alpha7-beta2-alpha7-beta2-alpha7 stoichiometry plus NACHO; this does not quantify native neuronal stoichiometry/distribution. Alpha6/3 comparator is a chimera. Antagonist allostery does not imply beta2 is an autonomous receptor.

Human full-length subunit recordings establish ACh-elicited single channels and stoichiometry-selective divalent potentiation. Cryo-EM resolves actual ACh density at alpha4-beta2 and alpha4-alpha interfaces. Structural full-length construct has Bril insertions and tag, alongside loop-deleted constructs. Calcium-site structural/mutational potentiation is not identical to calcium permeation; some sites arise from simulations alone. Alpha4 site mutations are not beta2 calcium-binding-site measurements.

The authentic abstract reports human alpha5 coassembly with beta2 in Xenopus oocytes and endogenous alpha5-associated receptors in SH-SY5Y cells; exact curated co-IP records independently preserve those contexts.

Authentic abstract explicitly describes human alpha2/alpha3/alpha4 paired with beta2 or beta4 in oocytes and ACh currents blocked by d-tubocurare. Original full Methods unavailable after the documented access attempts; supports assembled-receptor function, not free beta2 binding.

Mouse beta2 loss reduces nicotine antinociception and associated neuronal responses, supporting a contextual nociceptive-circuit contribution.

Mouse beta2/beta4 loss disrupts autonomic nicotinic signaling and bladder responses, whereas direct muscarinic contraction remains intact. The receptor contribution regulates contraction through the neuronal circuit.

Mouse beta2 deletion transiently delays refinement of individual retinal ganglion dendrites; initial coarse ON/OFF organization persists and later stratification approaches control patterns.

Mouse neuronal recordings connect beta2-containing receptors to acetylcholine currents and depolarization. These experiments are not direct B-cell proliferation measurements.

Mouse β2 deletion alters the reported cocaine-associated dopamine-turnover pattern; basal metabolic impairment is not established.

Loss of mouse beta2-dependent retinal activity disrupts retinofugal organization and visual performance; the receptor supplies activity rather than phototransduction chemistry.

Mouse beta2-null projections develop later local segregation but fail to establish normal eye-specific layers in the lateral geniculate nucleus.

Rat nicotinic-subunit electrophysiology supports cholinergic transmission by assembled beta-containing receptors; the conserved human inference is a receptor contribution.

Mouse beta2 loss changes flexible exploration and social behavior without a simple loss of elementary movement.

Mouse receptor immunoprecipitation, dopamine-release assays and neuronal recordings distinguish beta2-containing terminal and somatic receptor populations.

Mouse beta2-dependent retinal activity contributes to orderly visual projection development. The result does not assign beta2 an autonomous axon-building activity.

Rat heteromeric nicotinic receptors respond to acetylcholine in receptor-expression experiments, supporting the conserved agonist-response capability.

Beta2-null mice have altered REM-episode duration and stress-induced REM rebound despite similar overall baseline sleep-state amounts.

Adult beta2-null visual relay neurons have increased firing; the study leaves developmental and inhibitory-circuit explanations open rather than making the beta2 pore intrinsically inhibitory.

Mouse beta2 loss disrupts nicotine-mediated rescue of ethanol-associated learning effects; alpha7-dependent ethanol sensitivity is a separate result.

An alpha7/beta2 double-mutant mouse experiment links nicotinic receptors to passive avoidance, with the separate contribution of each deleted subunit unresolved.

Mouse alpha4/beta2 receptors stably expressed in human HEK293T cells produce agonist-evoked calcium responses, primarily from entry through the receptor with an additional intracellular-store contribution. This is receptor reconstitution, not an intact-mouse knockout experiment.

Combined beta2 and connexin36 perturbation alters early retinal activity but allows later local segregation, separating distinct activity-dependent stages.

Beta2-deficient mice have normal young-adult hearing followed by later hearing impairment and spiral-ganglion loss. The result supports auditory neuronal maintenance during aging rather than nerve development.

Mouse B-cell nicotinic-receptor experiments include beta2 deletion and context-dependent CD40/nicotine responses. The available abstract does not resolve the precise positive proliferation or activation interpretation.

Mouse knockout/chimera flow cytometry measures lymphocyte population sizes and B-cell precursor survival, including increased annexin-V-positive cells. The accessible abstract does not establish a separately measured B-cell activation assay.

Beta2 deletion and targeted reexpression alter mouse dopamine-neuron firing, linking cholinergic receptor activity to dopaminergic circuit regulation.

Young beta2-null superior-colliculus neurons receive more weak retinal inputs; mature animals have similar input number and strength to controls, indicating developmental refinement.

Rodent electrophysiology distinguishes presynaptic alpha6/beta2-dependent modulation of GABA release from predominantly postsynaptic alpha4/beta2 currents; knockout comparisons and rat recordings have distinct species scopes.

Lipid perturbations alter currents through rat alpha3/beta2 receptors expressed in hippocampal neurons. The experiments do not distinguish physical receptor redistribution from altered molecular interactions.

Mouse beta2 deletion abolishes nicotine-stimulated ventral-striatal dopamine release and neuronal nicotine currents, supporting a receptor-mediated contribution to nicotine responses.