Cannabidiol produces distinct U-shaped dose-response effects on cocaine conditioned place preference and associated recruitment of prelimbic neurons in male rats

Biological Psychiatry Global Open Science

2021 Jul 01

Nedelescu, H;Wagner, G;De Ness, G;Carrol, A;Kerr, T;Wang, J;Zhang, S;Chang, S;Than, A;Emerson, N;Suto, N;Weiss, F;
| DOI: 10.1016/j.bpsgos.2021.06.014

Background Cannabidiol (CBD) has received attention for the treatment of Substance Use Disorders. In preclinical models of relapse, CBD attenuates drug seeking across several drugs of abuse, including cocaine. However, in these models, CBD has not been consistently effective. This inconsistency in CBD effects may be related to presently insufficient information on the full spectrum of CBD dose effects on drug-related behaviors. Methods We address this issue by establishing a full dose-response profile of CBD’s actions using expression of cocaine-induced conditioned place preference (CPP) as a model for drug motivated behavior in male rats, and by concurrently identifying dose-dependent effects of CBD on underlying neuronal activation as well as distinct neuronal phenotypes showing dose-dependent activation changes. Additionally, CBD levels in plasma and brain were established. Results CBD produced linear increases in CBD brain/plasma concentrations but suppressed CPP in a distinct U-shaped manner. In parallel with its behavioral effects, CBD produced U-shaped suppressant effects on neuronal activation in the prelimbic but not infralimbic cortex or nucleus accumbens core and shell. RNAscope in situ hybridization identified suppression of glutamatergic and GABAergic signaling in the prelimbic cortex as a possible cellular mechanism for the attenuation of cocaine CPP by CBD. Conclusions The findings extend previous evidence on the potential of CBD in preventing drug motivated behavior. However, CBD’s dose-response profile may have important dosing implications for future clinical applications and may contribute to the understanding of discrepant CBD effects on drug seeking in the literature.

Evidence For and Against Direct Kidney Infection by SARS-CoV-2 in Patients with COVID-19

Clinical journal of the American Society of Nephrology : CJASN

2021 Jun 14

Hassler, L;Reyes, F;Sparks, M;Welling, P;Batlle, D;
PMID: 34127485 | DOI: 10.2215/CJN.04560421

Despite evidence of multi-organ tropism of SARS-CoV-2 in patients with COVID-19, direct viral kidney invasion has been difficult to demonstrate. The question of whether SARS-CoV-2 can directly infect the kidney is relevant to the understanding of pathogenesis of acute kidney injury and collapsing glomerulopathy in COVID-19. Methodologies to document SARS-CoV-2 infection that have been used include immunohistochemistry, immunofluorescence, reverse transcriptase polymerase chain reaction (RT-PCR), in situ hybridization and electron microscopy. In our review of studies to date we found that SARS-CoV-2 in the kidney of patients with COVID-19 was detected in 18 of 94 (19%) by immuno-histochemistry, 71 of 144 (49%) by RT-PCR and 11 of 84 (13%) by in situ hybridization. In a smaller number of patients with COVID-19 examined by immunofluorescence, SARS-CoV-2 was detected in 10 of 13 (77%). In total, in kidneys from 102 of 235 patients (43.4%), the presence of SARS-CoV-2 was suggested by at least one of the methods used. Despite these positive findings, caution is needed as many other studies have been negative for SARS-CoV-2 presence and it should be noted that when detected it was only in kidneys obtained at autopsy. There is a clear need for studies from kidney biopsies, including those performed at early stages of the COVID-19 associated kidney disease. Development of tests to detect kidney viral infection in urine samples would be more practical as a non-invasive way to evaluate SARS CoV-2 infection during the evolution of COVID-19-associated kidney disease.

Chronic pain‐mediated Regulator of G protein signaling 4 (RGS4) gene expression in superficial dorsal horn of spinal cord

The FASEB Journal

2021 Jan 01

Zimering, J;Pryce, K;Zachariou, V;
| DOI: 10.1096/fasebj.2021.35.S1.02365

Regulator of G protein signaling 4 (RGS4) is a potent negative regulator of G-protein coupled receptor signaling duration. Recent studies have identified RGS4 as a key gene in the maintenance of mechanical and cold allodynia associated with chronic pain states in mice. RGS4 is abundantly expressed across the pain matrix, and several studies have demonstrated upregulation of RGS4 mRNA in response to both peripheral inflammation and nerve injury. Here, we tested the hypothesis that peripheral nerve injury alters RGS4 neuronal expression broadly, and with specific expression-patterning among excitatory and inhibitory interneuron populations within the superficial dorsal horn of the mouse spinal cord. Chronic neuropathic pain was induced in C57BL/6 male mice via spared-nerve injury (SNI). At 2.5 months post-surgery (SNI vs sham), animals were sacrificed and lumbar spinal cords were harvested for tissue processing. RNAScope, an ultrasensitive RNA ISH method, was used to visualize and quantify single-molecule expression of RGS4, prodynorphin/PDYN (exclusively expressed by inhibitory dorsal horn interneurons), and somatostatin/SST (expressed by excitatory interneurons) within the cellular topography of the lumbar superficial dorsal horn. RGS4 expression increased significantly in the dorsal horn following spared-nerve injury (P =0.0384). RGS4 mRNA remained unchanged (SNI vs sham) among expression-positive dorsal horn neurons (p=0.6327). In sham-treated mice, there were no differences in cell-type specific (PDYN vs. SST) RGS4 expression patterns in the dorsal horn (p=0.4170). Cell-type specific RGS4 expression in the dorsal horn was significantly different (F (2,27) = 8.353; P =0.0015; one-way ANOVA) following spared-nerve injury. SNI-induced RGS4 expression was significantly enriched in PDYN vs SST-expressing interneurons (p=0.0300), and overall RGS4 expression was significantly downregulated in SST-expressing cells compared to all cells (p=0.0012). These data demonstrate that nerve injury induces upregulation of RGS4 in the superficial dorsal horn, and suggest that RGS4-positive inhibitory interneurons may be implicated in influencing persistent pain signaling within the dorsal horn of the spinal cord.

Cell type specific expression of soluble epoxide hydrolase protein and mRNA in human AMD and murine eyes with choroidal neovascularization

Investigative Ophthalmology & Visual Science

2021 Jan 01

Park, B;Qi, X;Boulton, ME;

Purpose : Soluble epoxide hydrolase (sEH) metabolizes pro-resolving epoxy fatty acids into diols. sEH is a potential therapeutic target for choroidal neovascularization (CNV) in wet age-related macular degeneration (AMD) and other eye diseases. Localization of sEH in the retina is contentious and cross-interpretation among different studies is complicated due to antibody limitations. This study aimed to define the localization of sEH through co-staining with retinal cell type markers and RNAscope in situ hybridization in human AMD and control eyes, and in mouse eyes with and without laser-induced CNV. Methods : Paraffin sections of eyes from anonymized human wet AMD and control subjects were obtained from the National Disease Research Interchange. 7-week old C57BL/6J mice underwent laser-induced CNV and on day 3 post laser, enucleated eyes were fixed and cryosectioned. Coimmunostaining was done for sEH, retinal pigment epithelium (RPE), and photoreceptor markers. RNAscope was performed using target specific probes for EPHX2 (encoding sEH) and images were acquired by confocal microscopy. Results : Costaining of sEH with cell type markers revealed that sEH is overexpressed in photoreceptors and RPE cells in areas with degenerative changes. By RNAscope, EPHX2 mRNA was also highly expressed in the pathological conditions compared to controls. EPHX2 mRNA was seen in the inner nuclear layer, outer nuclear layer and RPE of the normal and diseased human and mouse retina. Conclusions : Previous data showed sEH expression in vasculature, Müller glia, and inner and outer segments of photoreceptors. Here, we also revealed sEH protein and mRNA expression in the RPE. Overexpression of sEH at the protein and mRNA level in CNV and disease-relevant cell types indicates a functional role of sEH in AMD pathophysiology and provides a context to target these cell types for developing pharmacotherapies.

Activation of α 6-containing GABA A receptors induces antinociception under physiological and pathological conditions

Pain

2023 May 01

Rodríguez-Palma, EJ;De la Luz-Cuellar, YE;Islas-Espinoza, AM;Félix-Leyva, AE;Shiers, SI;García, G;Torres-López, JE;Delgado-Lezama, R;Murbartián, J;Price, TJ;Granados-Soto, V;
PMID: 36001074 | DOI: 10.1097/j.pain.0000000000002763

The loss of GABAergic inhibition is a mechanism that underlies neuropathic pain. Therefore, rescuing the GABAergic inhibitory tone through the activation of GABA A receptors is a strategy to reduce neuropathic pain. This study was designed to elucidate the function of the spinal α 6 -containing GABA A receptor in physiological conditions and neuropathic pain in female and male rats. Results show that α 6 -containing GABA A receptor blockade or transient α 6 -containing GABA A receptor knockdown induces evoked hypersensitivity and spontaneous pain in naive female rats. The α 6 subunit is expressed in IB4 + and CGRP + primary afferent neurons in the rat spinal dorsal horn and dorsal root ganglia but not astrocytes. Nerve injury reduces α 6 subunit protein expression in the central terminals of the primary afferent neurons and dorsal root ganglia, whereas intrathecal administration of positive allosteric modulators of the α 6 -containing GABA A receptor reduces tactile allodynia and spontaneous nociceptive behaviors in female, but not male, neuropathic rats and mice. Overexpression of the spinal α 6 subunit reduces tactile allodynia and restores α 6 subunit expression in neuropathic rats. Positive allosteric modulators of the α 6 -containing GABA A receptor induces a greater antiallodynic effect in female rats and mice compared with male rats and mice. Finally, α 6 subunit is expressed in humans. This receptor is found in CGRP + and P2X3 + primary afferent fibers but not astrocytes in the human spinal dorsal horn. Our results suggest that the spinal α 6 -containing GABA A receptor has a sex-specific antinociceptive role in neuropathic pain, suggesting that this receptor may represent an interesting target to develop a novel treatment for neuropathic pain.

The Slack Channel Regulates Anxiety-like Behaviors via Basolateral Amygdala Glutamatergic Projections to Ventral Hippocampus

The Journal of neuroscience : the official journal of the Society for Neuroscience

2022 Feb 22

Zhang, Q;Gao, SH;Shen, ZS;Wang, Y;Hu, SW;Duan, GB;Liu, Y;Zhong, DY;Liu, J;Sun, MH;Zhang, X;Cao, TY;Cao, JL;Tang, QY;Zhang, Z;
PMID: 35197318 | DOI: 10.1523/JNEUROSCI.2027-21.2022

Anxiety disorders are a series of mental disorders characterized by anxiety and fear, but the molecular basis of these disorders remains unclear. In the present study, we find that the global Slack KO male mice exhibit anxious behaviors whereas the Slack Y777H male mice manifest anxiolytic behaviors. The expression of Slack channels is rich in BLA glutamatergic neurons and down-regulated in chronic corticosterone-treated mice. In addition, electrophysiological data show enhanced excitability of BLA glutamatergic neurons in the Slack KO mice and decreased excitability of these neurons in the Slack Y777H mice. Furthermore, the Slack channel deletion in BLA glutamatergic neurons is sufficient to result in enhanced avoidance behaviors while Kcnt1 gene expression in the BLA or BLA-vHPC glutamatergic projections reverses anxious behaviors of the Slack KO mice. Our study identifies the role of the Slack channel in controlling anxious behaviors by decreasing the excitability of BLA-vHPC glutamatergic projections, providing a potential target for anxiolytic therapies.SIGNIFICANCE STATEMENTAnxiety disorders are a series of mental disorders characterized by anxiety and fear, but the molecular basis of these disorders remains unclear. Here, we examined the loss- and gain-of-function Slack channel mice's behaviors in elevated plus maze and open field tests and found the anxiolytic role of the Slack channel. By altering the Slack channel expression in the specific neuronal circuit, we demonstrated that the Slack channel played its anxiolytic role by decreasing the excitability of BLA-vHPC glutamatergic projections. Our data reveal the role of the Slack channel in the regulation of anxiety, which may provide a potential molecular target for anxiolytic therapies.

A prolactin-dependent sexually dimorphic mechanism of migraine chronification

Cephalalgia : an international journal of headache

2021 Sep 12

Ikegami, D;Navratilova, E;Yue, X;Moutal, A;Kopruszinski, CM;Khanna, R;Patwardhan, A;Dodick, DW;Porreca, F;
PMID: 34510920 | DOI: 10.1177/03331024211039813

Determination of possible sex differences in mechanisms promoting migraine progression and the contribution of prolactin and the prolactin long (PRLR-L) and short (PRLR-S) receptor isoforms.The majority of patients with chronic migraine and medication overuse headache are female. Prolactin is present at higher levels in women and increases migraine. Prolactin signaling at the PRLR-S selectively sensitizes nociceptors in female rodents, while expression of the PRLR-L is protective.Medication overuse headache was modeled by repeated sumatriptan administration in male and female mice. Periorbital and hindpaw cutaneous allodynia served as a surrogate of migraine-like pain. PRLR-L and PRLR-S isoforms were measured in the trigeminal ganglion with western blotting. Possible co-localization of PRLR with serotonin 5HT1B and 5HT1D receptors was determined with RNAscope. Cabergoline, a dopamine receptor agonist that inhibits circulating prolactin, was co-administered with sumatriptan. Nasal administration of CRISPR/Cas9 plasmid was used to edit expression of both PRLR isoforms.PRLR was co-localized with 5HT1B or 5HT1D receptors in the ophthalmic region of female trigeminal ganglion. A single injection of sumatriptan increased serum PRL levels in female mice. Repeated sumatriptan promoted cutaneous allodynia in both sexes but down-regulated trigeminal ganglion PRLR-L, without altering PRLR-S, only in females. Co-administration of sumatriptan with cabergoline prevented allodynia and down-regulation of PRLR-L only in females. CRISPR/Cas9 editing of both PRLR isoforms in the trigeminal ganglion prevented sumatriptan-induced periorbital allodynia in females.We identified a sexually dimorphic mechanism of migraine chronification that involves down-regulation of PRLR-L and increased signaling of circulating prolactin at PRLR-S. These studies reveal a previously unrecognized neuroendocrine mechanism linking the hypothalamus to nociceptor sensitization that increases the risk of migraine pain in females and suggest opportunities for novel sex-specific therapies including gene editing through nasal delivery of CRISPR/Cas9 constructs.

Empagliflozin Disrupts a Tnfrsf12a-Mediated Feed Forward Loop That Promotes Left Ventricular Hypertrophy

Cardiovascular drugs and therapy

2021 Apr 22

Yerra, VG;Batchu, SN;Kabir, G;Advani, SL;Liu, Y;Siddiqi, FS;Connelly, KA;Advani, A;
PMID: 33886003 | DOI: 10.1007/s10557-021-07190-2

Although the cardioprotective benefits of sodium-glucose cotransporter 2 (SGLT2) inhibitors are now widely appreciated, the mechanisms underlying these benefits remain unresolved. Tumor necrosis factor receptor superfamily member 12a (Tnfrsf12a) is a receptor for tumor necrosis factor superfamily member 12 (Tnfsf12). Tnfrsf12a is highly inducible and plays a key role in the development of cardiac hypertrophy and heart failure. Here we set out to determine if SGLT2 inhibition affects the Tnfsf12/Tnfrsf12a system in the stressed myocardium. C57BL/6N mice that had undergone sham or transverse aortic constriction (TAC) surgery were treated with either the SGLT2 inhibitor empagliflozin (400 mg/kg diet; 60-65 mg/kg/day) or standard chow alone and were followed for 8 weeks. Tnfrsf12a expression in mouse hearts was assessed by in situ hybridization, qRT-PCR, and immunoblotting. Left ventricular (LV) mass, end-systolic volume, and end-diastolic volume were all increased in TAC mice and were significantly lower with empagliflozin. Myocyte hypertrophy and interstitial fibrosis in TAC hearts were similarly attenuated with empagliflozin. Tnfrsf12a expression was upregulated in mouse hearts following TAC surgery but not in the hearts of empagliflozin-treated mice. In cultured cardiomyocytes, Tnfrsf12a antagonism attenuated the increase in cardiomyocyte size that was induced by phenylephrine. Empagliflozin attenuates LV enlargement in mice with hypertrophic heart failure. This effect may be mediated, at least in part, by a reduction in loading conditions which limits upregulation of the inducible, proinflammatory, and prohypertrophic TNF superfamily receptor, Tnfrsf12a. Disruption of the Tnfsf12/Tnfrsf12a feed forward system may contribute to the cardioprotective benefits of SGLT2 inhibition.

A basomedial amygdala to intercalated cells microcircuit expressing PACAP and its receptor PAC1 regulates contextual fear

The Journal of neuroscience : the official journal of the Society for Neuroscience

2021 Feb 26

Rajbhandari, AK;Octeau, JC;Gonzalez, S;Pennington, ZT;Mohamed, F;Trott, J;Chavez, J;Ngyuen, E;Keces, N;Hong, WZ;Neve, RL;Waschek, J;Khakh, BS;Fanselow, MS;
PMID: 33637560 | DOI: 10.1523/JNEUROSCI.2564-20.2021

Trauma can cause dysfunctional fear regulation leading some people to develop disorders such as post-traumatic stress disorder (PTSD). The amygdala regulates fear, whereas PACAP (pituitary adenylate activating peptide) and PAC1 receptors are linked to PTSD symptom severity at genetic/epigenetic levels, with a strong link in females with PTSD. We discovered a PACAPergic projection from the basomedial amygdala (BMA) to the medial intercalated cells (mICCs) in adult mice. In vivo optogenetic stimulation of this pathway increased cfos expression in mICCs, decreased fear recall and increased fear extinction. Selective deletion of PAC1 receptors from the mICCs in females reduced fear acquisition, but enhanced fear generalization and reduced fear extinction in males. Optogenetic stimulation of the BMA-mICCs PACAPergic pathway produced excitatory postsynaptic currents (EPSCs) in mICC neurons, which were enhanced by the PAC1 receptor antagonist, PACAP 6-38. Our findings show that mICCs modulate contextual fear in a dynamic and sex-dependent manner via a microcircuit containing the BMA and mICCs, and in a manner that was dependent on behavioral state.SIGNIFICANCE STATEMENTTraumatic stress can affect different aspects of fear behaviors including fear learning, generalization of learned fear to novel contexts, how the fear of the original context is recalled, and how fear is reduced over time. While the amygdala has been studied for its role in regulation of different aspects of fear, the molecular circuitry of this structure is quite complex. In addition, aspects of fear can be modulated differently in males and females. Our findings show that a specific circuitry containing the neuropeptide PACAP and its receptor, PAC1, regulates various aspects of fear including acquisition, generalization, recall and extinction in a sexually dimorphic manner, characterizing a novel pathway that modulates traumatic fear.

Expression of an alternatively spliced variant of SORL1 in neuronal dendrites is decreased in patients with Alzheimer\'s disease

Acta neuropathologica communications

2021 Mar 16

Monti, G;Kjolby, M;Jensen, AMG;Allen, M;Reiche, J;Møller, PL;Comaposada-Baró, R;Zolkowski, BE;Vieira, C;Jørgensen, MM;Holm, IE;Valdmanis, PN;Wellner, N;Vægter, CB;Lincoln, SJ;Nykjær, A;Ertekin-Taner, N;Young, JE;Nyegaard, M;Andersen, OM;
PMID: 33726851 | DOI: 10.1186/s40478-021-01140-7

SORL1 is strongly associated with both sporadic and familial forms of Alzheimer's disease (AD), but a lack of information about alternatively spliced transcripts currently limits our understanding of the role of SORL1 in AD. Here, we describe a SORL1 transcript (SORL1-38b) characterized by inclusion of a novel exon (E38b) that encodes a truncated protein. We identified E38b-containing transcripts in several brain regions, with the highest expression in the cerebellum and showed that SORL1-38b is largely located in neuronal dendrites, which is in contrast to the somatic distribution of transcripts encoding the full-length SORLA protein (SORL1-fl). SORL1-38b transcript levels were significantly reduced in AD cerebellum in three independent cohorts of postmortem brains, whereas no changes were observed for SORL1-fl. A trend of lower 38b transcript level in cerebellum was found for individuals carrying the risk variant at rs2282649 (known as SNP24), although not reaching statistical significance. These findings suggest synaptic functions for SORL1-38b in the brain, uncovering novel aspects of SORL1 that can be further explored in AD research.

Inhibition of transforming growth factor β1 signaling in resident interstitial cells attenuates profibrotic gene expression and preserves erythropoietin production during experimental kidney fibrosis in mice

Kidney international

2021 Mar 08

Fuchs, MAA;Broeker, KAE;Schrankl, J;Burzlaff, N;Willam, C;Wagner, C;Kurtz, A;
PMID: 33705825 | DOI: 10.1016/j.kint.2021.02.035

Kidney fibrosis is characterized by the development of myofibroblasts originating from resident kidney and immigrating cells. Myofibroblast formation and extracellular matrix production during kidney damage are triggered by various cytokines. Among these, transforming growth factor β1 (TGFβ1) is considered a central trigger for kidney fibrosis. We found a highly upregulated expression of TGFβ1 and TGFβ receptor 2 (TGFβ-R2) mRNAs in kidney interstitial cells in experimental fibrosis. Here, we investigated the contribution of TGFβ1 signaling in resident kidney interstitial cells to organ fibrosis using the models of adenine induced nephropathy and unilateral ureter occlusion in mice. For this purpose TGFβ1 signaling was interrupted by inducible deletion of the TGFβ-R2 gene in interstitial cells expressing the fibroblast marker platelet derived growth factor receptor-β. Expression of profibrotic genes was attenuated up to 50% in kidneys lacking TGFβ-R2 in cells positive for platelet derived growth factor receptor-β. Additionally, deletion of TGFβ-R2 prevented the decline of erythropoietin production in ureter ligated kidneys. Notably, fibrosis associated expression of α-smooth muscle actin as a myofibroblast marker and deposits of extracellular collagens were not altered in mice with targeted deletion of TGFβ-R2. Thus, our findings suggest an enhancing effect of TGFβ1 signaling in resident interstitial cells that contributes to profibrotic gene expression and the downregulation of erythropoietin production, but not to the development of myofibroblasts during kidney fibrosis.

Histamine H1 receptor deletion in cholinergic neurons induces sensorimotor gating ability deficit and social impairments in mice

Nature communications

2021 Feb 18

Cheng, L;Xu, C;Wang, L;An, D;Jiang, L;Zheng, Y;Xu, Y;Wang, Y;Wang, Y;Zhang, K;Wang, X;Zhang, X;Bao, A;Zhou, Y;Yang, J;Duan, S;Swaab, DF;Hu, W;Chen, Z;
PMID: 33602941 | DOI: 10.1038/s41467-021-21476-x

Negative symptoms in schizophrenia strongly contribute to poor functional outcomes, however its pathogenesis is still unclear. Here, we found that histamine H1 receptor (H1R) expression in basal forebrain (BF) cholinergic neurons was decreased in patients with schizophrenia having negative symptoms. Deletion of H1R gene in cholinergic neurons in mice resulted in functional deficiency of cholinergic projections from the BF to the prefrontal cortex and in the formation of sensorimotor gating deficit, social impairment and anhedonia-like behavior. These behavioral deficits can be rescued by re-expressing H1R or by chemogenetic activation of cholinergic neurons in the BF. Direct chemogenetic inhibition of BF cholinergic neurons produced such behavioral deficits and also increased the susceptibility to hyperlocomotion. Our results suggest that the H1R deficiency in BF cholinergic neurons is critical for sensorimotor gating deficit, social impairments and anhedonia-like behavior. This finding may help to understand the genetic and biochemical bases of negative symptoms in schizophrenia.

Pages

	Description
sense Example: Hs-LAG3-sense	Standard probes for RNA detection are in antisense. Sense probe is reverse complent to the corresponding antisense probe.
Intron# Example: Mm-Htt-intron2	Probe targets the indicated intron in the target gene, commonly used for pre-mRNA detection
Pool/Pan Example: Hs-CD3-pool (Hs-CD3D, Hs-CD3E, Hs-CD3G)	A mixture of multiple probe sets targeting multiple genes or transcripts
No-XSp Example: Hs-PDGFB-No-XMm	Does not cross detect with the species (Sp)
XSp Example: Rn-Pde9a-XMm	designed to cross detect with the species (Sp)
O# Example: Mm-Islr-O1	Alternative design targeting different regions of the same transcript or isoforms
CDS Example: Hs-SLC31A-CDS	Probe targets the protein-coding sequence only
EnEm	Probe targets exons n and m
En-Em	Probe targets region from exon n to exon m
Retired Nomenclature
tvn Example: Hs-LEPR-tv1	Designed to target transcript variant n
ORF Example: Hs-ACVRL1-ORF	Probe targets open reading frame
UTR Example: Hs-HTT-UTR-C3	Probe targets the untranslated region (non-protein-coding region) only
5UTR Example: Hs-GNRHR-5UTR	Probe targets the 5' untranslated region only
3UTR Example: Rn-Npy1r-3UTR	Probe targets the 3' untranslated region only
Pan Example: Pool	A mixture of multiple probe sets targeting multiple genes or transcripts

Search form

Probes for INS

Content for comparison

Gene

Product

Research area

Category

Pages

Advanced Cell Diagnostics

Bio-Techne

Advanced Cell Diagnostics China