Probes for INS
ACD can configure probes for the various manual and automated assays for INS for RNAscope Assay, or for Basescope Assay compatible for your species of interest.
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Methods in molecular biology (Clifton, N.J.)
2022 Jun 25
Aldana, R;Freed, D;
PMID: 35751805 | DOI: 10.1007/978-1-0716-2293-3_1
Public and private genomic sequencing initiatives generate ever-increasing amounts of genomic data creating a need for improved solutions for genomics data processing (Stephens et al.PLoS Biol 13:e1002195, 2015). The Sentieon Genomics software enables rapid and accurate analysis of next-generation sequence data. In this work, we present a typical use of the Sentieon Genomics software for germline variant calling. The Sentieon germline variant calling pipeline produces more accurate results than other tools on third-party benchmarks (Katherine et al. Front Genet 10:736, 2019; Shen et al. bioRxiv, 885517, 2019) in one tenth the time of comparable pipelines. Parts of this guide come from the official Sentieon Genomics software manual in https://support.sentieon.com/manual (Sentieon. Sentieon Genomics software manual, n.d.) and from the official Sentieon Genomics software application notes in https://support.sentieon.com/appnotes (Sentieon. Sentieon Genomics software application notes, n.d.) and are republished with permission. For additional details and advanced usage instructions of the Sentieon tools, refer to the software manual.
Nature communications
2022 May 04
Ghorbani, S;Jelinek, E;Jain, R;Buehner, B;Li, C;Lozinski, BM;Sarkar, S;Kaushik, DK;Dong, Y;Wight, TN;Karimi-Abdolrezaee, S;Schenk, GJ;Strijbis, EM;Geurts, J;Zhang, P;Ling, CC;Yong, VW;
PMID: 35508608 | DOI: 10.1038/s41467-022-30032-0
Remyelination failure in multiple sclerosis (MS) contributes to progression of disability. The deficient repair results from neuroinflammation and deposition of inhibitors including chondroitin sulfate proteoglycans (CSPGs). Which CSPG member is repair-inhibitory or alters local inflammation to exacerbate injury is unknown. Here, we correlate high versican-V1 expression in MS lesions with deficient premyelinating oligodendrocytes, and highlight its selective upregulation amongst CSPG members in experimental autoimmune encephalomyelitis (EAE) lesions modeling MS. In culture, purified versican-V1 inhibits oligodendrocyte precursor cells (OPCs) and promotes T helper 17 (Th17) polarization. Versican-V1-exposed Th17 cells are particularly toxic to OPCs. In NG2CreER:MAPTmGFP mice illuminating newly formed GFP+ oligodendrocytes/myelin, difluorosamine (peracetylated,4,4-difluoro-N-acetylglucosamine) treatment from peak EAE reduces lesional versican-V1 and Th17 frequency, while enhancing GFP+ profiles. We suggest that lesion-elevated versican-V1 directly impedes OPCs while it indirectly inhibits remyelination through elevating local Th17 cytotoxic neuroinflammation. We propose CSPG-lowering drugs as potential dual pronged repair and immunomodulatory therapeutics for MS.
Biological Psychiatry
2022 May 01
Dzirasa, K;Ransey, E;Chesnov, K;Wisdom, E;Bowman, R;Rodriguez, T;Adamson, E;Thomas, G;Almoril-Porras, A;Schwennesen, H;Colón-Ramos, D;Hultman, R;Bursac, N;
| DOI: 10.1016/j.biopsych.2022.02.055
Background The coordination of activity between brain cells is a key determinant of neural circuit function; nevertheless, approaches that selectively regulate communication between two distinct cellular components of a circuit, while leaving the activity of the presynaptic brain cell undisturbed remain sparse. Methods To address this gap, we developed a novel class of electrical synapses by selectively engineering two connexin proteins found in Morone americana (white perch fish): connexin34.7 (Cx34.7) and connexin35 (Cx35). Results By iteratively exploiting protein mutagenesis, a novel in vitro assay of connexin docking, and computational modeling of connexin hemichannel interactions, we uncovered the pattern of structural motifs that broadly determine connexin hemichannel docking. We then utilized this knowledge to design Cx34.7 and Cx35 hemichannels that dock with each other, but not with themselves nor other major connexins expressed in the human central nervous system. We validated these hemichannels in vivo, demonstrating that they facilitate communication between two neurons in Caenorhabditis elegans and recode a learned behavioral preference. Conclusions This system can be applied to edit circuits composed by pairs of genetically defined brain cell types across multiple species. Thus, we establish a potentially translational approach, ‘Long-term integration of Circuits using connexins’ (LinCx), for context-precise circuit-editing with unprecedented spatiotemporal specificity.
Fat3 Acts Through Independent Cytoskeletal Effectors to Coordinate Asymmetric Cell Behaviors During Polarized Circuit Assembly
SSRN Electronic Journal
2021 Sep 08
Aviles, E;Krol, A;Henle, S;Burroughs-Garcia, J;Deans, M;Goodrich, L;
| DOI: 10.2139/ssrn.3917159
The polarized flow of information through neural circuits depends on the orderly arrangement of neurons, their processes, and their synapses. This polarity emerges sequentially in development, starting with directed migration of neuronal precursors, which subsequently elaborate neurites that form synapses in specific locations. In other organs, Fat cadherins sense position and then polarize individual cells by inducing localized changes in the cytoskeleton that are coordinated across the tissue. Here, we show that the Fat-related protein Fat3 plays an analogous role during assembly of polarized circuits in the murine retina. We found that the Fat3 intracellular domain binds to cytoskeletal regulators and synaptic proteins, with discrete motifs required for amacrine cell migration and neurite retraction. Moreover, upon ICD deletion, extra neurites formed but did not make extra synapses, suggesting that Fat3 independently regulates synapse localization. Thus, Fat3 serves as a molecular node to coordinate asymmetric cell behaviors across development.
International journal of molecular sciences
2022 Feb 22
Helweg, LP;Windmöller, BA;Burghardt, L;Storm, J;Förster, C;Wethkamp, N;Wilkens, L;Kaltschmidt, B;Banz-Jansen, C;Kaltschmidt, C;
PMID: 35269569 | DOI: 10.3390/ijms23052426
Cancer stem cells (CSCs) are a small subpopulation of tumor cells harboring properties that include self-renewal, multi-lineage differentiation, tumor reconstitution, drug resistance and invasiveness, making them key players in tumor relapse. In the present paper, we develop new CSC models and analyze the molecular pathways involved in survival to identify targets for the establishment of novel therapies. Endometrial carcinoma-derived stem-like cells (ECSCs) were isolated from carcinogenic gynecological tissue and analyzed regarding their expression of prominent CSC markers. Further, they were treated with the MYC-signaling inhibitor KJ-Pyr-9, chemotherapeutic agent carboplatin and type II diabetes medication metformin. ECSC populations express common CSC markers, such as Prominin-1 and CD44 antigen as well as epithelial-to-mesenchymal transition markers, Twist, Snail and Slug, and exhibit the ability to form free-floating spheres. The inhibition of MYC signaling and treatment with carboplatin as well as metformin significantly reduced the cell survival of ECSC-like cells. Further, treatment with metformin significantly decreased the mitochondrial membrane potential of ECSC-like cells, while the extracellular lactate concentration was increased. The established ECSC-like populations represent promising in vitro models to further study the contribution of ECSCs to endometrial carcinogenesis. Targeting MYC signaling as well as mitochondrial bioenergetics has shown promising results in the diminishment of ECSCs, although molecular signaling pathways need further investigations.
Nature biotechnology
2022 Feb 07
Wagner, J;Olson, ND;Harris, L;McDaniel, J;Cheng, H;Fungtammasan, A;Hwang, YC;Gupta, R;Wenger, AM;Rowell, WJ;Khan, ZM;Farek, J;Zhu, Y;Pisupati, A;Mahmoud, M;Xiao, C;Yoo, B;Sahraeian, SME;Miller, DE;Jáspez, D;Lorenzo-Salazar, JM;Muñoz-Barrera, A;Rubio-Rodríguez, LA;Flores, C;Narzisi, G;Evani, US;Clarke, WE;Lee, J;Mason, CE;Lincoln, SE;Miga, KH;Ebbert, MTW;Shumate, A;Li, H;Chin, CS;Zook, JM;Sedlazeck, FJ;
PMID: 35132260 | DOI: 10.1038/s41587-021-01158-1
The repetitive nature and complexity of some medically relevant genes poses a challenge for their accurate analysis in a clinical setting. The Genome in a Bottle Consortium has provided variant benchmark sets, but these exclude nearly 400 medically relevant genes due to their repetitiveness or polymorphic complexity. Here, we characterize 273 of these 395 challenging autosomal genes using a haplotype-resolved whole-genome assembly. This curated benchmark reports over 17,000 single-nucleotide variations, 3,600 insertions and deletions and 200 structural variations each for human genome reference GRCh37 and GRCh38 across HG002. We show that false duplications in either GRCh37 or GRCh38 result in reference-specific, missed variants for short- and long-read technologies in medically relevant genes, including CBS, CRYAA and KCNE1. When masking these false duplications, variant recall can improve from 8% to 100%. Forming benchmarks from a haplotype-resolved whole-genome assembly may become a prototype for future benchmarks covering the whole genome.
Molecular therapy : the journal of the American Society of Gene Therapy
2022 Feb 02
Packer, MS;Chowdhary, V;Lung, G;Cheng, LI;Aratyn-Schaus, Y;Leboeuf, D;Smith, S;Shah, A;Chen, D;Zieger, M;Cafferty, BJ;Yan, B;Ciaramella, G;Gregoire, FM;Mueller, C;
PMID: 35121111 | DOI: 10.1016/j.ymthe.2022.01.040
Alpha-1 antitrypsin deficiency (AATD) is a rare autosomal codominant disease caused by mutations within the SERPINA1 gene. The most prevalent variant in patients is PiZ SERPINA1, containing a single G > A transition mutation. PiZ alpha-1 antitrypsin (AAT) is prone to misfolding, leading to the accumulation of toxic aggregates within hepatocytes. In addition, the abnormally low level of AAT secreted into circulation provides insufficient inhibition of neutrophil elastase within the lungs, eventually causing emphysema. Cytosine and adenine base editors enable the programmable conversion of C⋅G to T⋅A and A⋅T to G⋅C base pairs, respectively. In this study, two different base editing approaches were developed: use of a cytosine base editor to install a compensatory mutation (p.Met374Ile) and use of an adenine base editor to mediate the correction of the pathogenic PiZ mutation. After treatment with lipid nanoparticles formulated with base editing reagents, PiZ-transgenic mice exhibited durable editing of SERPINA1 in the liver, increased serum AAT, and improved liver histology. These results indicate that base editing has the potential to address both lung and liver disease in AATD.
Advances in Cancer Research
2022 Feb 24
Khatib, S;Wang, X;
| DOI: 10.1016/bs.acr.2022.01.006
Tumor heterogeneity is a major feature of primary liver cancers. Defined as the unique genotypic and phenotypic differences of cancer cells within a single tumor (intratumor) or amongst different patients (intertumor), tumor heterogeneity has consistently been linked to worse clinical outcomes in most, if not all, solid tumor types. In particular, liver cancer heterogeneity has been associated with altered immune infiltration, resistance to therapeutics, and worse overall patient survival. Current advancements in single-cell omic technologies have allowed for a deeper understanding and appreciation of the intricate composition and relationships between individual cells within a tumor. These observations have led to the discovery of new cell types in liver cancer, potential new mechanisms of therapy resistance and tumor progression, and new insights into the evolutionary patterns of liver cancer. To better understand the tumor biology of liver cancers and their heterogeneous features, we will begin this chapter on a brief background of liver cancer and then discuss the various etiologies of this disease and how each one can contribute to diverse genomic, transcriptomic, proteomic, and spatial architecture observations. Next, we will go into the specific causes and implications of tumor heterogeneity and end with how understanding the spatial architecture of liver tumors can provide us with new insights and ideas for tumor diversity and therapeutic development.
The AAPS journal
2022 Jan 31
Chen, N;Sun, K;Chemuturi, NV;Cho, H;Xia, CQ;
PMID: 35102450 | DOI: 10.1208/s12248-021-00678-7
Given the recent success of gene therapy modalities and the growing number of cell and gene-based therapies in clinical development across many different therapeutic areas, it is evident that this evolving field holds great promise for the unmet medical needs of patients. The recent approvals of Luxturna and Zolgensma prove that recombinant adeno-associated virus (rAAV)-based gene therapy is a transformative modality that enables curative treatment for genetic disorders. Over the last decade, Takeda has accumulated significant experience with rAAV-based gene therapies, especially in the early stage of development. In this review, based on the learnings from Takeda and publicly available information, we aim to provide a guiding perspective on Drug Metabolism and Pharmacokinetics (DMPK) substantial role in advancing therapeutic gene therapy modalities from nonclinical research to clinical development, in particular the characterization of gene therapy product biodistribution, elimination (shedding), immunogenicity assessment, multiple platform bioanalytical assays, and first-in-human (FIH) dose projection strategies. Graphical abstract.
Neuron
2021 Nov 17
Herz, J;Fu, Z;Kim, K;Dykstra, T;Wall, M;Li, H;Salvador, AF;Zou, B;Yan, N;Blackburn, SM;Andrews, PH;Goldman, DH;Papadopoulos, Z;Smirnov, I;Xie, XS;Kipnis, J;
PMID: 34793707 | DOI: 10.1016/j.neuron.2021.10.022
Mechanisms governing how immune cells and their derived molecules impact homeostatic brain function are still poorly understood. Here, we elucidate neuronal mechanisms underlying T cell effects on synaptic function and episodic memory. Depletion of CD4 T cells led to memory deficits and impaired long-term potentiation. Severe combined immune-deficient mice exhibited amnesia, which was reversible by repopulation with T cells from wild-type but not from IL-4-knockout mice. Behaviors impacted by T cells were mediated via IL-4 receptors expressed on neurons. Exploration of snRNA-seq of neurons participating in memory processing provided insights into synaptic organization and plasticity-associated pathways regulated by immune cells. IL-4Rα knockout in inhibitory (but not in excitatory) neurons was sufficient to impair contextual fear memory, and snRNA-seq from these mice pointed to IL-4-driven regulation of synaptic function in promoting memory. These findings provide new insights into complex neuroimmune interactions at the transcriptional and functional levels in neurons under physiological conditions.
Developmental cell
2021 Dec 20
Sun, X;Perl, AK;Li, R;Bell, SM;Sajti, E;Kalinichenko, VV;Kalin, TV;Misra, RS;Deshmukh, H;Clair, G;Kyle, J;Crotty Alexander, LE;Silva, JM;Kitzmiller, JA;Wikenheiser-Brokamp, KA;Deutsch, G;Guo, M;Du, Y;Morley, MP;Valdez, MJ;Yu, HV;Jin, K;Bardes, EE;Zepp, JA;Neithamer, T;Basil, MC;Zacharias, WJ;Verheyden, J;Young, R;Bandyopadhyay, G;Lin, S;Ansong, C;Adkins, J;Salomonis, N;Aronow, BJ;Xu, Y;Pryhuber, G;Whitsett, J;Morrisey, EE;NHLBI LungMAP Consortium, ;
PMID: 34936882 | DOI: 10.1016/j.devcel.2021.11.007
The human lung plays vital roles in respiration, host defense, and basic physiology. Recent technological advancements such as single-cell RNA sequencing and genetic lineage tracing have revealed novel cell types and enriched functional properties of existing cell types in lung. The time has come to take a new census. Initiated by members of the NHLBI-funded LungMAP Consortium and aided by experts in the lung biology community, we synthesized current data into a comprehensive and practical cellular census of the lung. Identities of cell types in the normal lung are captured in individual cell cards with delineation of function, markers, developmental lineages, heterogeneity, regenerative potential, disease links, and key experimental tools. This publication will serve as the starting point of a live, up-to-date guide for lung research at https://www.lungmap.net/cell-cards/. We hope that Lung CellCards will promote the community-wide effort to establish, maintain, and restore respiratory health.
American journal of respiratory cell and molecular biology
2021 Dec 03
Vu, LD;Phan, ATQ;Hijano, DR;Siefker, DT;Tillman, H;Cormier, SA;
PMID: 34861136 | DOI: 10.1165/rcmb.2021-0313OC
Respiratory syncytial virus (RSV)-induced immunopathogenesis and disease severity in neonatal mice and human infants have been related to elevated pulmonary IL-33. Thus, targeting IL-33 has been suggested as a potential therapy for respiratory viral infections. Yet, the regulatory mechanisms on IL-33 during early life remain unclear. Here, using a neonatal mouse model of RSV, we demonstrate that IL-1β positively regulates but is not required for RSV-induced expression of pulmonary IL-33 in neonatal mice early after the initial infection. Exogenous IL-1β upregulates RSV-induced IL-33 expression by promoting the proliferation of IL-33pos lung epithelial stem/progenitor cells (EpiSPC). These cells are exclusively detected in RSV-infected neonatal rather than adult mice, partially explaining the IL-1β-independent IL-33 expression in RSV-infected adult mice. Furthermore, IL-1β aggravates IL-33 mediated Th2 biased immunopathogenesis upon reinfection. Collectively, our study demonstrates that IL-1β exacerbates IL-33 mediated RSV immunopathogenesis by promoting the proliferation of IL-33pos EpiSPC in early life.
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| 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 | |
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