Capp pipette, variable vol. 0.1-2 ul, Bravo Capp Bravo variable volume (Minimum order 25 pipettes)
- Known as:
- Capp pipette, variable vol. 0.1-2 ul, Bravo Capp Bravo variable volume (Minimum order 25 pipettes)
- Catalog number:
- B02-1
- Category:
- -
- Supplier:
- Capp
- Gene target:
- Capp pipette variable vol. 0.1-2 Bravo volume (Minimum order 25 pipettes)
Related genes to: Capp pipette, variable vol. 0.1-2 ul, Bravo Capp Bravo variable volume (Minimum order 25 pipettes)
- Gene:
- ACOT13 NIH gene
- Name:
- acyl-CoA thioesterase 13
- Previous symbol:
- THEM2
- Synonyms:
- HT012
- Chromosome:
- 6p22.3
- Locus Type:
- gene with protein product
- Date approved:
- 2003-05-02
- Date modifiied:
- 2016-10-05
- Gene:
- AGAP4 NIH gene
- Name:
- ArfGAP with GTPase domain, ankyrin repeat and PH domain 4
- Previous symbol:
- CTGLF1, AGAP8, CTGLF5
- Synonyms:
- Em:AC012044.1, MRIP2
- Chromosome:
- 10q11.22
- Locus Type:
- gene with protein product
- Date approved:
- 2004-05-27
- Date modifiied:
- 2016-10-05
- Gene:
- ASB14 NIH gene
- Name:
- ankyrin repeat and SOCS box containing 14
- Previous symbol:
- -
- Synonyms:
- DKFZp313L0121
- Chromosome:
- 3p14.3
- Locus Type:
- gene with protein product
- Date approved:
- 2002-12-03
- Date modifiied:
- 2016-10-05
- Gene:
- ASPN NIH gene
- Name:
- asporin
- Previous symbol:
- -
- Synonyms:
- FLJ20129, SLRR1C, PLAP-1
- Chromosome:
- 9q22.31
- Locus Type:
- gene with protein product
- Date approved:
- 2001-03-21
- Date modifiied:
- 2017-07-14
- Gene:
- ATG16L2 NIH gene
- Name:
- autophagy related 16 like 2
- Previous symbol:
- -
- Synonyms:
- FLJ00012, WDR80, ATG16B
- Chromosome:
- 11q13.4
- Locus Type:
- gene with protein product
- Date approved:
- 2005-09-13
- Date modifiied:
- 2015-11-24
Related products to: Capp pipette, variable vol. 0.1-2 ul, Bravo Capp Bravo variable volume (Minimum order 25 pipettes)
Related articles to: Capp pipette, variable vol. 0.1-2 ul, Bravo Capp Bravo variable volume (Minimum order 25 pipettes)
- Wound healing after spinal cord injury involves highly coordinated interactions among multiple cell types, which are poorly understood. Astrocytes play a central role in creating a border against the non-neural lesion core. To do so, astrocytes undergo dramatic morphological changes by first thickening and elongating their processes and then overlapping them to form a physical barrier. We show here that the expression of a cell-surface receptor, Ryk, is induced in astrocytes after injury in both rodent and human spinal cords. Astrocyte-specific knockout of dramatically elongated the reactive astrocytes, accelerated the formation of the border, and reduced the size of the scar. Astrocyte-specific knockout of also accelerated the injury responses of multiple cell types. Single-cell transcriptomics analyses revealed a broad range of changes in cell signaling among astrocytes, microglia, fibroblasts, and endothelial cells after astrocyte-specific knockout, suggesting that Ryk not only regulates injury responses of astrocytes but may also regulate signals emanating from astrocytes and coordinate the responses of these cell types. The elongation of astrocyte processes is mediated by NrCAM, a cell adhesion molecule induced by astrocyte-specific conditional knockout of after spinal cord injury. Our findings suggest that Ryk is a promising therapeutic target to accelerate wound healing, promote neuronal survival, and enhance functional recovery. - Source: PubMed
Publication date: 2025/04/10
Shen ZheFeng BoLim Wei LingWoo TimothyLiu YanlinVicenzi SilviaWang JingyiKwon Brian KZou Yimin - To overcome the paucity of known tumor-specific surface antigens in pediatric high-grade glioma (pHGG), we contrasted splicing patterns in pHGGs and normal brain samples. Among alternative splicing events affecting extracellular protein domains, the most pervasive alteration was the skipping of ≤30 nucleotide-long microexons. Several of these skipped microexons mapped to L1-IgCAM family members, such as . Bulk and single-nuclei short- and long-read RNA-seq revealed uniform skipping of microexons 5 and 19 in virtually every pHGG sample. Importantly, the Δex5Δex19 (but not the full-length) NRCAM proteoform was essential for pHGG cell migration and invasion in vitro and tumor growth in vivo. We developed a monoclonal antibody selective for Δex5Δex19 NRCAM and demonstrated that "painting" of pHGG cells with this antibody enables killing by T cells armed with an FcRI-based universal immune receptor. Thus, pHGG-specific NRCAM and possibly other L1-IgCAM proteoforms are promising and highly selective targets for adoptive immunotherapies. - Source: PubMed
Publication date: 2025/01/19
Sehgal PriyankaNaqvi Ammar SHiggins MakennaLiu JiagengHarvey KyraJarroux JulienKim TaewooMankaliye BerkMishra PamelaWatterson GraceFine JustynDavis JacintaHayer Katharina ECastro AnnetteMogbo AdannaDrummer CharlesMartinez DanielKoptyra Mateusz PAng ZhiweiWang KaiFarrel AlvinQuesnel-Vallieres MathieuBarash YosephSpangler Jamie BRokita Jo LynneResnick Adam CTilgner Hagen UDeRaedt ThomasPowell Daniel JThomas-Tikhonenko Andrei - The perisomatic region of cortical pyramidal neurons (PNs) integrates local and long-range inputs and regulates firing. This domain receives GABAergic inputs from cholecystokinin (CCK)- and Parvalbumin (PV)-expressing basket cells (BCs) but how synaptic contacts are established is unclear. Neuron-glial related cell adhesion molecule (NrCAM) is a homophilic transmembrane protein that binds the scaffold protein Ankyrin B. Here we show that NrCAM and Ankyrin B mediate perisomatic synaptic contact between CCK-BCs and PNs in mouse medial prefrontal cortex (mPFC). Immunolabeling of CCK-BC terminals for vesicular glutamate transporter-3 (VGLUT3) or vesicular GABA transporter (VGAT) revealed a significant decrease in CCK-BC synaptic puncta on PN soma in NrCAM-null mice, however no decrease in PV-BC puncta or cell loss. VGLUT3+ CCK-BC puncta were also decreased by Ankyrin B deletion from PNs in Nex1Cre-ERT2:Ank2 :EGFP mice. A novel CCK-BC reporter mouse expressing tdTomato (tdT) at the Synuclein-γ ( ) locus showed NrCAM localized to Sncg+ CCK-BCs, and to postsynaptic PN soma in Nex1Cre-ERT2:Ank2 :EGFP mice. Results suggest that NrCAM and Ankyrin B contribute to the establishment of connectivity between CCK-BCs and excitatory neurons of the mPFC. - Source: PubMed
Publication date: 2025/03/10
Oldre Erik NWebb Barrett DSperringer Justin EManess Patricia F - The transparent ocular lens is essential for vision because it focuses light onto the retina. Despite recognition of the importance of its unique cellular architecture and mechanical properties, the molecular mechanisms governing these attributes remain elusive. This study aims to elucidate the role of ankyrin-B (AnkB, encoded by ANK2), a membrane scaffolding protein, in lens cytoarchitecture, growth and function using a conditional knockout (cKO) mouse model. The AnkB cKO mouse has no defects in lens morphogenesis but exhibited changes that supported a global role for AnkB in maintenance of lens clarity, size, cytoarchitecture, membrane organization and stiffness. Notably, absence of AnkB led to nuclear cataract formation, which was evident from postnatal day 16. AnkB cKO lens fibers exhibit progressive disruption in membrane organization of the spectrin-actin cytoskeleton, cell adhesion proteins and channel proteins; loss and degradation of several membrane proteins [such as NrCAM. N-cadherin (CDH2) and aquaporin-0 (also known as MIP)]; along with a disorganized plasma membrane and impaired membrane interdigitations. Furthermore, absence of AnkB led to decreased lens stiffness. Collectively, these results illustrate the essential role for AnkB in lens architecture, growth and function through its involvement in membrane skeletal and protein organization and stability. - Source: PubMed
Publication date: 2024/12/18
Maddala RupalathaAllen ArianaSkiba Nikolai PRao Ponugoti Vasantha - Wound healing after spinal cord injury involves highly coordinated interactions among multiple cell types, which is poorly understood. Astrocytes play a central role in creating a border against the non-neural lesion core. To do so, astrocytes undergo dramatic morphological changes by first thickening the processes and then elongating and overlap them. We show here show that the expression of a cell-surface receptor, Ryk, is induced in astrocytes after injury in both rodent and human spinal cord. Astrocyte-specific knockout of Ryk dramatically elongated the reactive astrocytes and accelerated the formation of the border and reduced the size of the scar. Astrocyte-specific knockout of Ryk also accelerated the injury responses of multiple cell types, including the resolution of neuroinflammation. Single cell transcriptomics analyses revealed a broad range of changes cell signaling among astrocytes, microglia, fibroblasts, endothelial cell, etc, after astrocyte-specific Ryk knockout, suggesting that Ryk not only regulates the injury response of astrocytes but may also regulate signals which coordinate the responses of multiple cell types. The elongation is mediated by NrCAM, a cell adhesion molecule induced by astrocyte-specific conditional knockout of Ryk after spinal cord injury. Our findings suggest a promising therapeutic target to accelerate wound healing and promote neuronal survival and enhance functional recovery. - Source: PubMed
Publication date: 2024/10/18
Shen ZheFeng BoLim Wei LingWoo TimothyLiu YanlinVicenzi SilviaWang JingyiKwon Brian KZou Yimin