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mitochondria to acceptor cells1-3. One possible consequence of mitochondria
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mitochondria, which was mediated by tethering of mitochondria-lysosome contact
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mitochondria with normal function. In addition, the half-life of mitochondria
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Mitochondria shape is controlled by membrane fusion and fission mediated
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Generate reviewed cross-disease analogy hypotheses from hypothesis:hypothesis-h-0e614ae4 and persist valuable results through substrate APIs.
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Generate reviewed cross-disease analogy hypotheses from hypothesis:hypothesis-h-22d2cfcd and persist valuable results through substrate APIs.
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Generate reviewed cross-disease analogy hypotheses from hypothesis:hypothesis-h-26b9f3e7 and persist valuable results through substrate APIs.
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Generate reviewed cross-disease analogy hypotheses from hypothesis:hypothesis-h-6726853448 and persist valuable results through substrate APIs.
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Generate reviewed cross-disease analogy hypotheses from hypothesis:hypothesis-h-e3e8407c and persist valuable results through substrate APIs.
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Generate reviewed cross-disease analogy hypotheses from hypothesis:hypothesis-h-var-6957745fea and persist valuable results through substrate APIs.
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Generate reviewed cross-disease analogy hypotheses from hypothesis:hypothesis-hyp-lyso-snca-c9e088045c26 and persist valuable results through substrate APIs.
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mitochondria respiration conferred resilience against stress-induced mitochondria damaging and epithelium
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mitochondria, inner segment dimensions, and optical properties, as a basis
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mitochondria-associated ER membrane fraction under starvation conditions. Disruption of the ER-mitochondria
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mitochondria and has been shown to play a central role
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mitochondria, respectively. Transgenic up-regulation of mitochondria-targeted CAPN1 dose
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mitochondria for degradation by autophagosomes. We examined the role of optineurin
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mitochondria-ER contact sites (MERCS). Upon damage, mitochondria produce reactive
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mitochondria to trigger their autophagy. How Parkin recognizes damaged mitochondria
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mitochondria. Failure to supply a sufficient amount of energy, seen
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Design a research-only SS-31-like peptide candidate that may stabilize cardiolipin-rich mitochondrial inner membranes. Context: - This is for SciDEX v2 beta testing and should be treated as a hypothesis-generating artifact, not medical advice or a therapeutic recommendation. - SS-31/elamipretide evidence to consider: - PMID 23813215 / DOI 10.1681/ASN.2012121216: SS-31 interacts with cardiolipin and protects cristae in an ischemia model. - PMID 32273339 / DOI 10.1074/jbc.RA119.012094: SS-31 binds lipid bilayers and modulates surface electrostatics. - PMID 35913044 / DOI 10.7554/eLife.75531: tetrapeptide structure-activity relationships for alternating aromatic/cationic mitochondrial compounds. - PubChem CID 11764719: elamipretide molecular metadata. Create these files in the current workspace: - lab_notes.md: intermediate notes, assumptions, source refs, rejected alternatives, risks, assay ideas. - design_description.md: description of the proposed peptide artifact. - descriptor_score.py: small deterministic descriptor/scoring script for aromatic/cationic balance, sequence length, and flags. - manifest.json: machine-readable summary with candidate id, canonical sequence surrogate, modified sequence notation, sources, and next experiments. Candidate constraints: - Prefer a short SS-31-like aromatic-cationic peptidomimetic. - Use a canonical amino-acid surrogate sequence that can fit a SciDEX protein_design artifact. - Make uncertainty explicit. - Avoid dosing, administration instructions, or claims of efficacy. Return a concise summary and list all files created.
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mitochondria into the neuronal milieu. The amount of damaged mitochondria
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Mitochondria transfer is a spontaneous process that releases functional mitochondria
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mitochondria downstream of PARK2, and induces autophagosome assembly around mitochondria
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mitochondria in 2-9 μ saccular structures (spheroids). Damaged mitochondria
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Mitochondria-associated membranes (MAMs) is a platform facilitating calcium transport
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mitochondria between heterogeneous cell types has been confirmed in various
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mitochondria, individual mitochondria were photolabeled and tracked through fusion and fission
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mitochondria is essential to neuronal homeostasis. Mitophagy is a critical
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mitochondria. Increasing Miro1 expression levels recruits Grif-1 to mitochondria
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