A1715 AP reverse primer(for integration diagnostics of all (R)AP(R) expression vectors with 5'utr aprt)
- Known as:
- A1715 AP reverse primer(to measure integration diagnostics (R)AP(R) expression vectors 5'utr aprt)
- Catalog number:
- PM-111
- Product Quantity:
- 2,5nmol
- Category:
- -
- Supplier:
- Jena Bio
- Gene target:
- A1715 reverse primer(for integration diagnostics all ()() expression vectors with 5'utr aprt)
Related genes to: A1715 AP reverse primer(for integration diagnostics of all (R)AP(R) expression vectors with 5'utr aprt)
- Gene:
- A1BG-AS1 NIH gene
- Name:
- A1BG antisense RNA 1
- Previous symbol:
- NCRNA00181, A1BGAS, A1BG-AS
- Synonyms:
- FLJ23569
- Chromosome:
- 19q13.43
- Locus Type:
- RNA, long non-coding
- Date approved:
- 2009-07-20
- Date modifiied:
- 2013-06-27
- Gene:
- A1CF NIH gene
- Name:
- APOBEC1 complementation factor
- Previous symbol:
- -
- Synonyms:
- ACF, ASP, ACF64, ACF65, APOBEC1CF
- Chromosome:
- 10q11.23
- Locus Type:
- gene with protein product
- Date approved:
- 2007-11-23
- Date modifiied:
- 2016-10-05
- Gene:
- A2M NIH gene
- Name:
- alpha-2-macroglobulin
- Previous symbol:
- -
- Synonyms:
- FWP007, S863-7, CPAMD5
- Chromosome:
- 12p13.31
- Locus Type:
- gene with protein product
- Date approved:
- 1986-01-01
- Date modifiied:
- 2018-05-03
- Gene:
- A2ML1 NIH gene
- Name:
- alpha-2-macroglobulin like 1
- Previous symbol:
- CPAMD9
- Synonyms:
- FLJ25179, p170
- Chromosome:
- 12p13.31
- Locus Type:
- gene with protein product
- Date approved:
- 2005-07-20
- Date modifiied:
- 2018-04-17
- Gene:
- A2MP1 NIH gene
- Name:
- alpha-2-macroglobulin pseudogene 1
- Previous symbol:
- A2MP
- Synonyms:
- -
- Chromosome:
- 12p13.31
- Locus Type:
- pseudogene
- Date approved:
- 1991-09-12
- Date modifiied:
- 2016-08-22
Related products to: A1715 AP reverse primer(for integration diagnostics of all (R)AP(R) expression vectors with 5'utr aprt)
(all-cis)-7,10,13,16,19-Docosapentaenoic Acid C22H34O2 CAS: 24880-45-3(all-cis)-7,10,13,16,19-Docosapentaenoic Acid CAS: 24880-45-3 Formula: C22H34O2 (all-cis)-7,10,13,16,19-Docosapentaenoic Acid N-Hydroxysuccinimidyl Ester CAS: Formula: C26H37NO4(all-cis)-7,10,13,16,19-Docosapentaenoic-d5 Acid CAS: Formula: C22H29D5O2(all-cis)-8,11,14,17-Eicosatetraenoic Acid C20H32O2 CAS: 24880-40-8
(all-cis)-8,11,14,17-Eicosatetraenoic Acid CAS: 24880-40-8
Formula: C20H32O2 (all-cis)-8,11,14,17-Eicosatetraenoic Acid N-Hydroxysuccinimidyl Ester CAS: Formula: C24H35NO4(all-Z)-5,8,11,14-Eicosatetraenylphosphonofluoridic Acid Methyl Ester CAS: 188404-10-6 Formula: C21H36FO2P(all-Z)-6,9,12,15,18-Heneicosapentaenoic Acid
C21H32O2 CAS: 24257-10-1(all-Z)-6,9,12,15,18-Heneicosapentaenoic Acid
CAS: 24257-10-1 Formula: C21H32O2 (all-Z)-6,9,12,15,18-Heneicosapentaenoic Acid Ethyl Ester C23H36O2 CAS: 131775-86-5(all-Z)-6,9,12,15,18-Heneicosapentaenoic Acid Ethyl Ester CAS: 131775-86-5 Formula: C23H36O2 (all-Z)-6,9,12,15,18-Heneicosapentaenoic Acid N-Succinimide
CAS: Formula: C25H35NO4(all-Z)-6,9,12,15,18-Heneicosapentaenoic-d5 Acid
CAS: Formula: C21H27D5O2*Lactobacillus MRS Broth (MRS Broth) USE For cultivation of all Lactobacilli. Related articles to: A1715 AP reverse primer(for integration diagnostics of all (R)AP(R) expression vectors with 5'utr aprt)
- The oriental river prawn () is an economically important aquaculture species in China. - Source: PubMed
Publication date: 2026/07/28
Hu ZhiguoWu YuyuanLiu JiahuiGuo XushengDuan Baohua - Homozygous loss-of-function mutations in LNPK, the gene encoding the endoplasmic reticulum-associated protein lunapark, have previously been linked to an autosomal recessive neurodevelopmental syndrome. Here, we describe an individual harboring compound heterozygous predicted splice site mutations with an overall matching phenotype. In cultured fibroblasts, these mutations result in a dearth of transcript and severe loss of protein, thereby establishing their likely pathogenicity. The underlying reduction in gene expression is due to the activation of the nonsense-mediated decay (NMD) pathway as a consequence of exon skipping rather than intron retention, leading to aberrant transcripts. We further demonstrate that cells from the affected individual and her mother exhibit a significant increase in transcript compared with a control cell line when treated with an inhibitor of NMD, suggesting potential genetic compensation. Together, this report describes disease-causing variants in LNPK and reveals their impact on transcription and mRNA stability. - Source: PubMed
Publication date: 2025/11/06
Doss Rose MWirth Sara APitsch Jonathan WDias Caroline MGropman Andrea LBreuss Martin W - Parkinson's disease (PD) has a complex genetic etiology, with autosomal recessive (AR) genes significantly contributing. This study uses next-generation sequencing (NGS) and long-read sequencing data (LRS) in Chinese AR-PD families to uncover novel genes, enhancing our genetic comprehension of PD. - Source: PubMed
Publication date: 2025/09/17
Zhao YuwenPan HongxuWang YigeChen JuanGuan HaoyuRen ZuowenZhou XiaoxiaXiang YaqinWu HengTan JieqiongSun QiyingXu QianWang JunlingShen LuJiang HongYan XinxiangLi JinchenGuo JifengLiu ZhenhuaTang Beisha - Misassembly of nucleoporins (Nups), central components of the nuclear pore complex (NPC), leads to Nup mislocalization outside of the nuclear envelope. Here we elucidate the fate of mislocalized Nups. To impair Nup assembly, we depleted the structural component Nup98 and found that nucleo-cytoplasmic transport by NPCs remains largely intact. Under this condition, several phenylalanine-glycine-rich Nups (FG-Nups) no longer assemble at the nuclear envelope but instead accumulate at discrete puncta in the endoplasmic reticulum (ER), which we term ER foci. Formation of the foci harboring the misassembled FG-Nups requires the ER morphogenic proteins RTN3, ATL3, and LNP (also known as LNPK). Preventing accumulation of misassembled FG-Nups at the ER foci impairs NPC nucleo-cytoplasmic transport, likely by allowing the misassembled FG-Nups to reach the nuclear envelope, where they disrupt NPC function. Formation of the ER foci is dependent on the kinesin-1 motor. Our results suggest that the ER can sequester misassembled Nups to help maintain NPC function. Because Nup mislocalization is found in many age-related neurodegenerative diseases, our data should illuminate the molecular basis of these pathologic conditions. - Source: PubMed
Publication date: 2025/03/25
Pletan MadisonWang EmilyGohmann LukeTsai Billy - encodes a conserved membrane protein that stabilizes the junctions of the tubular endoplasmic reticulum network playing crucial roles in diverse biological functions. Recently, homozygous variants in were shown to cause a neurodevelopmental disorder (OMIM#618090) in four patients displaying developmental delay, epilepsy and nonspecific brain malformations including corpus callosum hypoplasia and variable impairment of cerebellum. We sought to delineate the molecular and phenotypic spectrum of -related disorder. Exome or genome sequencing was carried out in 11 families. Thorough clinical and neuroradiological evaluation was performed for all the affected individuals, including review of previously reported patients. We identified 12 distinct homozygous loss-of-function variants in 16 individuals presenting with moderate to profound developmental delay, cognitive impairment, regression, refractory epilepsy and a recognizable neuroimaging pattern consisting of corpus callosum hypoplasia and signal alterations of the forceps minor ('ear-of-the-lynx' sign), variably associated with substantia nigra signal alterations, mild brain atrophy, short midbrain and cerebellar hypoplasia/atrophy. In summary, we define the core phenotype of -related disorder and expand the list of neurological disorders presenting with the 'ear-of-the-lynx' sign suggesting a possible common underlying mechanism related to endoplasmic reticulum-phagy dysfunction. - Source: PubMed
Publication date: 2023/08/17
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