The research report should be a detailed narrative explaining the function, biological processes, and localization of the gene product. Citations should be given for all claims.
You should prioritize authoritative reviews and primary scientific literature when conducting research. You can supplement
this with annotations you find in gene/protein databases, but these can be outdated or inaccurate.
We are specifically interested in the primary function of the gene - for enzymes, what reaction is catalyzed, and what is the substrate specificity? For transporters, what is the substrate? For structural proteins or adapters, what is the broader structural role? For signaling molecules, what is the role in the pathway.
We are interested in where in or outside the cell the gene product carries out its function.
We are also interested in the signaling or biochemical pathways in which the gene functions. We are less interested in broad pleiotropic effects, except where these elucidate the precise role.
Include evidence where possible. We are interested in both experimental evidence as well as inference from structure, evolution, or bioinformatic analysis. Precise studies should be prioritized over high-throughput, where available.
UniProt A0A0P6JY17 is coherently identified as naked-mole-rat Tac1, encoding protachykinin-1, a secreted neuropeptide precursor in the tachykinin family. The supplied InterPro/Pfam annotations—Tachykinin domain/family, Tachy_Neuro_lke_CS, and PF02202—fit this identity. This is not the distinct Tac2 gene, which encodes neurokinin B.
The most defensible primary annotation is: Tac1 produces precursor peptide(s) that are proteolytically processed into extracellular tachykinin ligands, principally substance P (SP), which signal through cell-surface neurokinin receptors. In the naked mole-rat, the coding locus is apparently intact, but SP expression is selectively absent from cutaneous peptidergic C-fibers. Consequently, a normally SP-dependent skin pain/itch pathway is functionally silent even though peripheral stimulus detection and downstream spinal NK1/NMDA machinery remain available. This selective expression defect—not loss of the receptor pathway—is supported by direct rescue experiments. Molecular processing details beyond SP, including production of neurokinin A (NKA), remain substantially inferred from other mammals rather than demonstrated for A0A0P6JY17.
| Annotation question | Best-supported conclusion | Evidence type | Confidence or caveat |
|---|---|---|---|
| Is UniProt A0A0P6JY17 the correct Heterocephalus glaber Tac1 protein? | Yes. The supplied record is consistent with H. glaber Tac1 / protachykinin-1, a tachykinin-family precursor; naked-mole-rat genomic literature also reports an intact TAC1 encoding substance P. | H. glaber genomics | High; identity is coherent across UniProt description and naked-mole-rat genome papers, but the report relies on the provided UniProt accession plus genome-level statements rather than a dedicated naked-mole-rat biochemical characterization of A0A0P6JY17 itself. (brand2010functionalneurokininand pages 1-2) |
| What is the primary molecular function of Tac1? | Tac1 encodes a secreted neuropeptide precursor rather than an enzyme or transporter. Its biological role is to be proteolytically processed into tachykinin signaling peptides that activate neurokinin receptors. | Mammalian orthology | High for mammals broadly; direct H. glaber molecular processing data are limited. (sanchez2023peptidergicsystemsand pages 2-5, humes2024substancep’simpact pages 1-2, zhu2023inflammationandorgan pages 2-4, campo2022tachykininsnewplayers pages 2-4) |
| Which peptide products are most likely generated from H. glaber Tac1? | At minimum, the precursor is expected to yield substance P (SP); by mammalian orthology it likely can also generate neurokinin A (NKA) and extended peptides such as NPK/NPγ, depending on transcript structure and processing. | Mammalian orthology + H. glaber genomics | Moderate; SP is directly tied to intact naked-mole-rat TAC1, whereas NKA/NPK/NPγ are inferred from conserved mammalian TAC1 splicing/processing and have not been directly demonstrated here in H. glaber. (sanchez2023peptidergicsystemsand pages 2-5, zhu2023inflammationandorgan pages 2-4, campo2022tachykininsnewplayers pages 2-4) |
| Where is the gene product expected to localize before release? | Conserved mammalian evidence supports synthesis in neurons, storage in dense-core vesicles, axonal transport, and regulated secretion at nerve terminals. | Mammalian orthology | Moderate to high for conserved TAC1 biology; not directly shown in the cited naked-mole-rat studies. (humes2024substancep’simpact pages 1-2) |
| Where is SP absent or present in naked mole-rat tissues? | The strongest direct evidence indicates absence of substance P in cutaneous C-fibers / small-diameter skin sensory neurons, while SP/CGRP-positive presumptive visceral sensory fibers have been reported, implying the loss is not global across all sensory afferents. | Direct H. glaber experiment | High for cutaneous absence; moderate for visceral presence because the cited evidence describes presumptive visceral sensory fibers rather than exhaustive tissue mapping. (brand2010functionalneurokininand pages 5-6, brand2010functionalneurokininand pages 1-2, smith2010absenceofhistamineinduced pages 1-2, zhao2025lifewithoutsubstance pages 5-8) |
| What pathway-level phenotype follows this cutaneous SP loss? | Naked mole-rats have a non-functional peptidergic cutaneous pain/itch pathway despite preserved activation of some peripheral nociceptors; this helps explain blunted capsaicin-, acid-, ammonia-, and histamine-linked behaviors. | Direct H. glaber experiment | High for the behavioral/physiological phenotype; the pathway label summarizes multiple studies. (browe2020thenakedmolerat pages 3-4, brand2010functionalneurokininand pages 1-2, smith2010absenceofhistamineinduced pages 1-2, smith2010absenceofhistamineinduced pages 3-5) |
| Are downstream spinal neurokinin mechanisms still functional in H. glaber? | Yes. Spinal NK1/NMDA signaling machinery is functional: intrathecal SP produces immediate or delayed heat sensitization depending on dose, and antagonists can reverse the SP-induced effect. | Direct H. glaber experiment | High; this is one of the best-supported mechanistic conclusions in the species. (brand2010functionalneurokininand pages 1-2, brand2010functionalneurokininand pages 2-4) |
| Can SP reintroduction rescue missing behaviors? | Yes. Exogenous or restored SP can rescue capsaicin-related pain behaviors/heat sensitization and histamine-evoked scratching in naked mole-rats. Quantitatively, intrathecal SP increased histamine-evoked scratching to 42.5 ± 7.0 bouts/20 min vs 1.0 ± 0.4 with saline; some heat-sensitization experiments used n=6 and histamine rescue experiments used N=4 groups. | Direct H. glaber experiment | High, but details differ by paradigm (intrathecal peptide vs viral preprotachykinin expression). (brand2010functionalneurokininand pages 2-4, smith2010absenceofhistamineinduced pages 1-2, smith2010absenceofhistamineinduced pages 3-5, zhao2025lifewithoutsubstance pages 8-12) |
| Which receptors are the likely primary targets of H. glaber TAC1 peptides? | By conserved mammalian evidence, SP preferentially activates NK1/TACR1, while NKA preferentially activates NK2/TACR2. | Mammalian orthology | High for receptor preference in mammals; only NK1-related function is directly demonstrated in the naked-mole-rat rescue studies summarized here. (sanchez2023peptidergicsystemsand pages 2-5, humes2024substancep’simpact pages 1-2, zhu2023inflammationandorgan pages 2-4, campo2022tachykininsnewplayers pages 2-4) |
| What intracellular signaling pathway is most likely engaged? | The best-supported conserved inference is Gq-coupled neurokinin receptor signaling, activating PLC/IP3/Ca2+ pathways downstream of SP/NKA receptor binding. | Mammalian orthology | Moderate; this is standard tachykinin receptor biology but was not directly dissected for H. glaber Tac1 in the retrieved species-specific studies. (humes2024substancep’simpact pages 1-2) |
| Is there a relevant 2023-2024 development for TAC1-derived peptides? | Yes. A 2023 study described CAP-TAC1, a capped TAC1-derived circulating peptide that is a nanomolar agonist at multiple tachykinin receptors and shows greater plasma stability than SP (half-life 17.1 min vs 8.5 min). | Recent non-H. glaber development | Moderate relevance for annotation; important as a new TAC1-derived signaling concept, but it has not been shown in naked mole-rat in the cited material. (wiggenhorn2023aclassof pages 1-2, wiggenhorn2023aclassof pages 6-7) |
Table: This table summarizes what can be concluded about Heterocephalus glaber Tac1 with explicit separation of direct naked-mole-rat evidence from mammalian orthology and recent non-species-specific developments. It is useful for functional annotation because it highlights both strong conclusions and the main caveats.
The target specified by the supplied UniProt record is A0A0P6JY17, protachykinin-1, gene Tac1, from Heterocephalus glaber. The designation agrees with naked-mole-rat genomic literature reporting an intact TAC1 locus associated with substance P biology. The tachykinin-family domains supplied by UniProt are appropriate for a short secreted prepropeptide containing conserved bioactive tachykinin segments; they do not indicate enzymatic or transporter activity.
Accordingly, the extensive mammalian literature on TAC1/protachykinin-1 is relevant for orthology-based interpretation, whereas literature on Tac2/TAC2, tachykinin receptors, or similarly named unrelated proteins cannot be treated as direct evidence for this protein.
A0A0P6JY17 appears to be computationally annotated rather than a purified, biochemically characterized naked-mole-rat protein. Direct literature on the accession itself is extremely limited. This report therefore distinguishes:
Protachykinin-1 is a prepropeptide substrate for the regulated secretory pathway. Mammalian TAC1 transcripts are alternatively spliced into four major precursor isoforms. All contain the sequence for the 11-residue SP peptide; selected isoforms also contain the 10-residue NKA sequence and can yield the extended products neuropeptide K and neuropeptide γ. Proteolytic cleavage at basic sites and peptidylglycine α-amidating monooxygenase-dependent C-terminal amidation generate mature bioactive tachykinins. Thus, “substrate specificity” or a catalytic reaction does not apply to Tac1 itself: it is the substrate from which receptor agonists are produced (sanchez2023peptidergicsystemsand pages 2-5, zhu2023inflammationandorgan pages 2-4, campo2022tachykininsnewplayers pages 2-4).
For A0A0P6JY17 specifically, SP is the best-supported product. Production of NKA or extended NKA peptides is biologically plausible from mammalian conservation but should remain annotated as predicted until naked-mole-rat transcript isoforms and endogenous processed peptides are established by long-read RNA sequencing and targeted peptidomics.
SP preferentially activates TACR1/NK1R, whereas NKA and its extended products preferentially activate TACR2/NK2R. These are seven-transmembrane class-A GPCRs (sanchez2023peptidergicsystemsand pages 2-5, humes2024substancep’simpact pages 1-2, campo2022tachykininsnewplayers pages 2-4). Conserved neurokinin-receptor signaling is primarily Gq/11-linked, activating phospholipase C, IP3-dependent intracellular Ca²⁺ mobilization, and downstream excitability and transcriptional responses. In nociceptive circuits, released SP therefore acts as a neuromodulator that strengthens postsynaptic transmission rather than serving as the initial detector of noxious stimuli.
Recent reviews also emphasize SP signaling through NK1R and, in some inflammatory contexts, MRGPRX2 or its rodent homolog. These broader inflammatory mechanisms are established outside the naked mole-rat and should not be assigned to A0A0P6JY17 without species-specific receptor and cellular evidence (zhu2023inflammationandorgan pages 2-4).
In conserved mammalian biology, TAC1 precursor is synthesized through the endoplasmic-reticulum/Golgi secretory pathway, processed, packaged into large dense-core vesicles, and transported rapidly along axons to nerve terminals. Injury or inflammatory activity triggers extracellular release into synaptic or neuroeffector spaces. SP is especially associated with small- and medium-diameter sensory neurons and central regions including the spinal dorsal horn; extracellular peptide acts on receptors on adjacent neurons, vascular or immune cells rather than functioning in the cytosol (humes2024substancep’simpact pages 1-2).
Signal termination includes extracellular degradation by peptidases such as neprilysin. Ligand–NK1R complexes can undergo endocytosis, after which SP is degraded in acidic intracellular compartments (zhu2023inflammationandorgan pages 2-4).
Direct immunolabeling shows that naked mole-rat small-diameter unmyelinated cutaneous sensory fibers lack detectable SP, along with CGRP, despite retaining distinct C-fiber populations (zhao2025lifewithoutsubstance pages 1-5, zhao2025lifewithoutsubstance pages 5-8). This should not be generalized to complete organism-wide absence: SP- and CGRP-positive presumptive sensory fibers have been reported in visceral tissues, suggesting tissue- or neuronal-subtype-specific regulation (brand2010functionalneurokininand pages 5-6).
The appropriate localization annotation is therefore:
Naked-mole-rat C-fibers can respond physiologically to capsaicin, indicating that upstream TRPV1-dependent stimulus detection remains intact. Nevertheless, animals show little or no capsaicin-evoked nocifensive behavior and lack several forms of thermal sensitization normally supported by SP release. They also show markedly reduced histamine-evoked scratching even though cultured DRG neurons respond to histamine. These dissociations localize the major defect downstream of peripheral stimulus detection, at the level of peptidergic afferent transmission and dorsal-horn processing (brand2010functionalneurokininand pages 1-2, smith2010absenceofhistamineinduced pages 3-5, zhao2025lifewithoutsubstance pages 5-8).
The phenotype is selective rather than generalized analgesia. Mechanical and basal thermal responses remain, and a purinergic/nonpeptidergic C-fiber pathway is functional. In formalin experiments, naked mole-rats and mice were tested at n=8 per species, with significantly reduced phase-I response time in naked mole-rats (p<0.01) (browe2020thenakedmolerat pages 3-4).
The strongest evidence comes from gain-of-function rescue:
These interventions provide stronger causal evidence than expression correlations: loss of endogenous cutaneous SP is sufficient to explain an important component of the sensory phenotype, while ligand replacement restores downstream output.
In experiments with n=6 animals, topical capsaicin at 1 or 10 mM did not sensitize heat withdrawal in naked mole-rats. Intrathecal SP at 1–10 mM produced delayed sensitization at approximately 60 minutes, while 100 mM produced immediate sensitization maintained for 120 minutes. The NMDA-receptor antagonist APV reversed SP-induced sensitization, supporting functional coupling between SP-sensitive spinal signaling and NMDA-dependent sensitization. SP- or NMDA-receptor antagonists alone did not alter baseline withdrawal in naïve animals, indicating that this pathway is available but not tonically recruited without endogenous SP (brand2010functionalneurokininand pages 1-2, brand2010functionalneurokininand pages 2-4).
Concentrations reported in these spinal experiments are pharmacological and should not be interpreted as physiological tissue levels.
A parsimonious pathway for cutaneous signaling is:
Noxious or pruritic stimulus → activation of peripheral C-fiber ion channels/receptors → activity-dependent SP release from central afferent terminals → NK1R activation in the superficial dorsal horn → enhancement of NMDA-dependent postsynaptic excitability → pain sensitization or itch behavior.
In the naked mole-rat, the pathway is interrupted chiefly at the SP production/release step in cutaneous C-fibers. The intact peripheral responses to capsaicin or histamine and successful intrathecal rescue argue against global failure of sensory transduction or postsynaptic receptor signaling (brand2010functionalneurokininand pages 1-2, smith2010absenceofhistamineinduced pages 1-2, smith2010absenceofhistamineinduced pages 3-5).
The proposed evolutionary interpretation is that reduced cutaneous peptidergic signaling may be adaptive in crowded subterranean burrows rich in CO₂ and ammonia, stimuli that would chronically activate or irritate trigeminal and cutaneous afferents in other mammals. This remains an evolutionary hypothesis rather than a direct molecular demonstration of selective pressure (zhao2025lifewithoutsubstance pages 1-5, brand2010functionalneurokininand pages 5-6).
A 2023 review of naked-mole-rat physiology reaffirmed that SP reintroduction can rescue capsaicin pain, placing Tac1-related signaling among the mechanisms underlying this species' unusual chemical-pain tolerance. The contemporary consensus is not that the animal lacks all pain, but that specific acid-sensitive and peptidergic pathways are altered while other sensory channels remain functional.
Broader 2023–2024 reviews continue to position the SP–NK1 system at the interface of pain, neurogenic inflammation, organ injury, and neuroimmune signaling. These sources support the conserved pathway interpretation but do not directly demonstrate additional A0A0P6JY17 functions in naked mole-rats (humes2024substancep’simpact pages 1-2, zhu2023inflammationandorgan pages 2-4).
A 2023 Nature Communications study identified CAP-TAC1, an N-terminally pyroglutamylated and C-terminally amidated TAC1-derived circulating peptide. It acted as a nanomolar agonist at multiple mammalian tachykinin receptors and was detected by targeted mass spectrometry in mouse and human plasma; estimated mouse concentrations ranged approximately 0.1–100 nM (wiggenhorn2023aclassof pages 1-2).
CAP-TAC1 was more stable in plasma than classical SP, with reported half-lives of 17.1 versus 8.5 minutes, respectively; CAP-TAC1 remained detectable after 60 minutes while SP did not (wiggenhorn2023aclassof pages 6-7). This expands the possible functional output of mammalian TAC1 beyond classical SP/NKA peptides. However, CAP-TAC1 has not been demonstrated in H. glaber, so it is a research priority rather than a present annotation for A0A0P6JY17.
The naked mole-rat supplies a natural “ligand-deficient but receptor-competent” system. Unlike a complete receptor knockout, it permits investigators to restore SP acutely and test circuit causality. This has already been implemented using intrathecal peptide delivery and viral precursor expression to dissect capsaicin pain, heat sensitization, histamine itch, and NMDA-dependent spinal plasticity (brand2010functionalneurokininand pages 2-4, smith2010absenceofhistamineinduced pages 1-2, zhao2025lifewithoutsubstance pages 8-12).
The model can inform strategies that reduce pathological SP release or interrupt NK1-dependent sensitization while preserving nonpeptidergic protective sensation. More broadly, SP/NK1 signaling is investigated in pain, inflammation, psychiatric conditions, and cancer. Nevertheless, these are pathway-level applications, not evidence that naked-mole-rat Tac1 or A0A0P6JY17 is currently used as a therapeutic product. No direct clinical implementation targeting this accession was identified.
High-confidence conclusions:
Moderate-confidence, orthology-based conclusions:
Principal gaps: direct A0A0P6JY17 proteomics; isoform-resolved naked-mole-rat Tac1 transcripts; comprehensive central, visceral, immune, and developmental expression maps; identification of the regulatory lesion suppressing cutaneous expression; and testing for endogenous CAP-TAC1. The most decisive next experiments would combine long-read sensory-neuron transcriptomics, single-cell/spatial RNA analysis, targeted amidated-peptide mass spectrometry, and receptor pharmacology using naked-mole-rat TACR1/TACR2.
Tac1/A0A0P6JY17 encodes a tachykinin prepropeptide whose conserved primary role is production of secreted neurokinin-receptor agonists, especially substance P. In naked-mole-rat skin sensory circuitry, suppression of endogenous SP in cutaneous C-fibers removes a critical neuromodulatory signal required for normal capsaicin-associated sensitization and histamine itch. The mature ligand normally acts extracellularly at spinal NK1 receptors to enhance NMDA-dependent neuronal excitation; downstream responsiveness is retained and can be experimentally rescued.
References
(brand2010functionalneurokininand pages 1-2): Antje Brand, Ewan St. J. Smith, Gary R. Lewin, and Thomas J. Park. Functional neurokinin and nmda receptor activity in an animal naturally lacking substance p: the naked mole-rat. PLoS ONE, 5:e15162, Dec 2010. URL: https://doi.org/10.1371/journal.pone.0015162, doi:10.1371/journal.pone.0015162. This article has 24 citations and is from a peer-reviewed journal.
(sanchez2023peptidergicsystemsand pages 2-5): Manuel Lisardo Sánchez, Francisco D. Rodríguez, and Rafael Coveñas. Peptidergic systems and cancer: focus on tachykinin and calcitonin/calcitonin gene-related peptide families. Mar 2023. URL: https://doi.org/10.3390/cancers15061694, doi:10.3390/cancers15061694. This article has 23 citations.
(humes2024substancep’simpact pages 1-2): Charles Humes, Aleksandar Sic, and Nebojsa Nick Knezevic. Substance p’s impact on chronic pain and psychiatric conditions—a narrative review. International Journal of Molecular Sciences, 25(11):5905, May 2024. URL: https://doi.org/10.3390/ijms25115905, doi:10.3390/ijms25115905. This article has 53 citations.
(zhu2023inflammationandorgan pages 2-4): Zhixing Zhu and Madhav Bhatia. Inflammation and organ injury the role of substance p and its receptors. International Journal of Molecular Sciences, 24:6140, Mar 2023. URL: https://doi.org/10.3390/ijms24076140, doi:10.3390/ijms24076140. This article has 32 citations.
(campo2022tachykininsnewplayers pages 2-4): Aurora Campo, Sylvie Dufour, and Karine Rousseau. Tachykinins, new players in the control of reproduction and food intake: a comparative review in mammals and teleosts. Frontiers in Endocrinology, Dec 2022. URL: https://doi.org/10.3389/fendo.2022.1056939, doi:10.3389/fendo.2022.1056939. This article has 25 citations.
(brand2010functionalneurokininand pages 5-6): Antje Brand, Ewan St. J. Smith, Gary R. Lewin, and Thomas J. Park. Functional neurokinin and nmda receptor activity in an animal naturally lacking substance p: the naked mole-rat. PLoS ONE, 5:e15162, Dec 2010. URL: https://doi.org/10.1371/journal.pone.0015162, doi:10.1371/journal.pone.0015162. This article has 24 citations and is from a peer-reviewed journal.
(smith2010absenceofhistamineinduced pages 1-2): Ewan St John Smith, Gregory RC Blass, Gary R Lewin, and Thomas J Park. Absence of histamine-induced itch in the african naked mole-rat and "rescue" by substance p. Molecular Pain, 6:29-29, Jan 2010. URL: https://doi.org/10.1186/1744-8069-6-29, doi:10.1186/1744-8069-6-29. This article has 55 citations and is from a peer-reviewed journal.
(zhao2025lifewithoutsubstance pages 5-8): Aishi Zhao, Jiwon Lee, Weronika Gryszkiewicz, and Thomas J. Park. Life without substance P: The naked mole rat, pages 275-290. Elsevier, Jan 2025. URL: https://doi.org/10.1016/b978-0-443-22194-1.00013-6, doi:10.1016/b978-0-443-22194-1.00013-6. This article has 0 citations.
(browe2020thenakedmolerat pages 3-4): Brigitte M Browe, Abigail R Olsen, Cesar Ramirez, Rebecca H Rickman, Ewan St John Smith, and Thomas J Park. The naked mole-rat has a functional purinergic pain pathway despite having a non-functional peptidergic pain pathway. Neurobiology of Pain, May 2020. URL: https://doi.org/10.1016/j.ynpai.2020.100047, doi:10.1016/j.ynpai.2020.100047. This article has 11 citations.
(smith2010absenceofhistamineinduced pages 3-5): Ewan St John Smith, Gregory RC Blass, Gary R Lewin, and Thomas J Park. Absence of histamine-induced itch in the african naked mole-rat and "rescue" by substance p. Molecular Pain, 6:29-29, Jan 2010. URL: https://doi.org/10.1186/1744-8069-6-29, doi:10.1186/1744-8069-6-29. This article has 55 citations and is from a peer-reviewed journal.
(brand2010functionalneurokininand pages 2-4): Antje Brand, Ewan St. J. Smith, Gary R. Lewin, and Thomas J. Park. Functional neurokinin and nmda receptor activity in an animal naturally lacking substance p: the naked mole-rat. PLoS ONE, 5:e15162, Dec 2010. URL: https://doi.org/10.1371/journal.pone.0015162, doi:10.1371/journal.pone.0015162. This article has 24 citations and is from a peer-reviewed journal.
(zhao2025lifewithoutsubstance pages 8-12): Aishi Zhao, Jiwon Lee, Weronika Gryszkiewicz, and Thomas J. Park. Life without substance P: The naked mole rat, pages 275-290. Elsevier, Jan 2025. URL: https://doi.org/10.1016/b978-0-443-22194-1.00013-6, doi:10.1016/b978-0-443-22194-1.00013-6. This article has 0 citations.
(wiggenhorn2023aclassof pages 1-2): Amanda L. Wiggenhorn, Hind Z. Abuzaid, Laetitia Coassolo, Veronica L. Li, Julia T. Tanzo, Wei Wei, Xuchao Lyu, Katrin J. Svensson, and Jonathan Z. Long. A class of secreted mammalian peptides with potential to expand cell-cell communication. Dec 2023. URL: https://doi.org/10.1038/s41467-023-43857-0, doi:10.1038/s41467-023-43857-0. This article has 27 citations and is from a highest quality peer-reviewed journal.
(wiggenhorn2023aclassof pages 6-7): Amanda L. Wiggenhorn, Hind Z. Abuzaid, Laetitia Coassolo, Veronica L. Li, Julia T. Tanzo, Wei Wei, Xuchao Lyu, Katrin J. Svensson, and Jonathan Z. Long. A class of secreted mammalian peptides with potential to expand cell-cell communication. Dec 2023. URL: https://doi.org/10.1038/s41467-023-43857-0, doi:10.1038/s41467-023-43857-0. This article has 27 citations and is from a highest quality peer-reviewed journal.
(zhao2025lifewithoutsubstance pages 1-5): Aishi Zhao, Jiwon Lee, Weronika Gryszkiewicz, and Thomas J. Park. Life without substance P: The naked mole rat, pages 275-290. Elsevier, Jan 2025. URL: https://doi.org/10.1016/b978-0-443-22194-1.00013-6, doi:10.1016/b978-0-443-22194-1.00013-6. This article has 0 citations.