Human Polyclonal NOTCH2 Ab
- Known as:
- Human Polyclonal NOTCH2 Antibody
- Catalog number:
- a0560
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- ABclonal
- Gene target:
- Human Polyclonal NOTCH2
Related genes to: Human Polyclonal NOTCH2 Ab
- Gene:
- NOTCH2 NIH gene
- Name:
- notch receptor 2
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 1p12
- Locus Type:
- gene with protein product
- Date approved:
- 1994-11-10
- Date modifiied:
- 2019-01-03
- Gene:
- NOTCH2NLA NIH gene
- Name:
- notch 2 N-terminal like A
- Previous symbol:
- NOTCH2NL
- Synonyms:
- N2N
- Chromosome:
- 1q21.1
- Locus Type:
- gene with protein product
- Date approved:
- 2004-12-02
- Date modifiied:
- 2018-08-01
Related products to: Human Polyclonal NOTCH2 Ab
Related articles to: Human Polyclonal NOTCH2 Ab
- NOTCH2NL (NOTCH2-N-terminus-like) genes arose from ape-specific chromosome 1 segmental duplications implicated in human brain cortical expansion, including an incomplete NOTCH2 gene. Genetic characterization of these loci and their regulation is complicated because they are embedded in large, nearly identical duplications that predispose to recurrent microdeletion syndromes. Using near-complete long-read assemblies generated from 70 human and 12 ape haploid genomes, we show independent recurrent duplication among apes with protein-coding copies emerging in humans 2.2-3.7 million years ago. We distinguish NOTCH2NL paralogs present in every human haplotype (NOTCH2NLA) from copy-number-variable ones. We also characterize large-scale structural variation, including gene conversion, for 28% of haplotypes, leading to a previously undescribed paralog, NOTCH2tv. Finally, we apply Fiber-seq and long-read transcript sequencing to human dorsal forebrain organoids to characterize the regulatory landscape and find that the most fixed paralogs, NOTCH2 and NOTCH2NLA, harbor the greatest number of paralog-specific elements potentially driving their regulation. - Source: PubMed
Publication date: 2026/03/30
Real Taylor DHebbar PrajnaYoo DongAhnAntonacci FrancescaPačar IvanaDubocanin DaniloDiekhans MarkMikol Gregory JPopoola Oyeronke GMallory Benjamin JVollger Mitchell RDishuck Philip CGuitart XaviRozanski Allison NMunson Katherine MHoekzema KendraRanchalis Jane ENeph Shane JSedeño-Cortés Adriana EPaten BenedictSalama Sofie RStergachis Andrew BEichler Evan E - (-N-terminus-like) genes arose from incomplete, recent chromosome 1 segmental duplications implicated in human brain cortical expansion. Genetic characterization of these loci and their regulation is complicated by the fact they are embedded in large, nearly identical duplications that predispose to recurrent microdeletion syndromes. Using nearly complete long-read assemblies generated from 67 human and 12 ape haploid genomes, we show independent recurrent duplication among apes with functional copies emerging in humans ~2.1 million years ago. We distinguish paralogs present in every human haplotype () from copy number variable ones. We also characterize large-scale structural variation, including gene conversion, for 28% of haplotypes leading to a previously undescribed paralog, Finally, we apply Fiber-seq and long-read transcript sequencing to human cortical neurospheres to characterize the regulatory landscape and find that the most fixed paralogs, and , harbor the greatest number of paralog-specific elements potentially driving their regulation. - Source: PubMed
Publication date: 2025/03/17
Real Taylor DHebbar PrajnaYoo DongAhnAntonacci FrancescaPačar IvanaDiekhans MarkMikol Gregory JPopoola Oyeronke GMallory Benjamin JVollger Mitchell RDishuck Philip CGuitart XaviRozanski Allison NMunson Katherine MHoekzema KendraRanchalis Jane ENeph Shane JSedeño-Cortes Adriana EPaten BenedictSalama Sofie RStergachis Andrew BEichler Evan E - This study was intended to delineate the profile of double-negative T cells (DNTs) in NOD.Cg-Prkdc Il2rg /SzJ mice and cytokines released from DNTs in vivo and in vitro. Total 4 × 10 cells of RC1012 injection per mice were intravenously infused. IFN-γ, TNF-α, IL-1β, IL-2, IL-4, IL-6, IL-10 were measured in vivo and in vitro. A quantitative polymerase chain reaction (PCR) was employed to determine the gene copies of Notch2-NLA per DNT cell from collected organs. Cytokines were significantly increased in vitro (4 h) and in vivo (3 h). DNT cells were distributed into the lung, liver, heart, and kidney earlier, and redistributed to lymphocyte homing spleen and bone marrow, which seemed to frame a two-compartment pharmacokinetics (PK) model but more data are needed to confirm this, and the clearance of DNT cells fell into first-order kinetics. - Source: PubMed
Publication date: 2021/07/03
Xu ShangzhiGe XinyuWang LiuyangTao YiminTang DongmeiDeng XiaojieYang FeiZhang QianQi XinmingGong LikunYang Liming - Over the past few years, human-specific genes have received increasing attention as potential major contributors responsible for the 3-fold difference in brain size between human and chimpanzee. Accordingly, mutations affecting these genes may lead to a reduction in human brain size and therefore, may cause or contribute to microcephaly. In this review, we will concentrate, within the brain, on the cerebral cortex, the seat of our higher cognitive abilities, and focus on the human-specific gene and on the gene family comprising the three human-specific genes , , and . These genes are thought to have significantly contributed to the expansion of the cerebral cortex during human evolution. We will summarize the evolution of these genes, as well as their expression and functional role during human cortical development, and discuss their potential relevance for microcephaly. Furthermore, we will give an overview of other human-specific genes that are expressed during fetal human cortical development. We will discuss the potential involvement of these genes in microcephaly and how these genes could be studied functionally to identify a possible role in microcephaly. - Source: PubMed
Publication date: 2021/05/15
Heide MichaelHuttner Wieland B