Ac_ IgG(H+L) hum GLOX
- Known as:
- Ac_ Immunoglobulin G(H+L) hum GLOX
- Catalog number:
- BI 1006
- Product Quantity:
- 4mg/2ml
- Category:
- -
- Supplier:
- P.A.R.I.S
- Gene target:
- Ac_ IgG(+) hum GLOX
Ask about this productRelated genes to: Ac_ IgG(H+L) hum GLOX
- Gene:
- HPDL NIH gene
- Name:
- 4-hydroxyphenylpyruvate dioxygenase like
- Previous symbol:
- GLOXD1
- Synonyms:
- MGC15668, 4-HPPD-L
- Chromosome:
- 1p34.1
- Locus Type:
- gene with protein product
- Date approved:
- 2005-07-26
- Date modifiied:
- 2016-03-16
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- Hereditary Spastic Paraplegia (HSP) is a rare neurodegenerative disorder causing progressive weakness and spasticity in the lower limbs. variants in the HPDL gene are linked to Spastic Paraplegia 83 (SPG83), an autosomal recessive form of HSP. While HPDL variants are known to cause SPG83, the molecular mechanisms behind its role remains unclear, mostly due to rare nature of the condition. - Source: PubMed
Publication date: 2026/05/11
Vaghefi FatemehKhosravi TeymoorMotallebi FarzanehZarghami SheydaAl Sudani Zainab MRahimzadeh ArianKowsari AliSefidbakht YahyaDolatabadi Alireza KargarOladnabi Morteza - Meyer of the Araliaceae family have various biological activities and pharmacological actions such as anticancer, immunomodulation, and anti-inflammatory. In many studies on ginseng, studies on ginseng fruit are still new, and the effect and potential of ginseng fruit on periodontitis in HPDL cells have been investigated and - Source: PubMed
Publication date: 2026/02/21
Lee Da EunKim Eun-NamTrang Nguyen MinhKim Jong HanKoo Gi-BangJung You HeeJeong Gil-Saeng - Primary coenzyme Q10 (CoQ10) deficiency results from mutations in genes involved in the CoQ10 biosynthetic pathway. In humans, at least 10 genes (, to ) are required for the biosynthesis of functional CoQ10, a mutation in any one of which can result in a deficit in CoQ10 status and present as primary CoQ10 deficiency. Furthermore, the genes and , whilst not part of the , to gene sequence, have also been shown to have a crucial role in CoQ10 biosynthesis. A major problem in treating primary CoQ10 deficiencies is the poor bioavailability of supplemental CoQ10, both in terms of lack of absorption from the digestive tract and inability to cross the human blood-brain barrier. Bypass strategies aim to circumvent this problem by using more bioavailable precursor analogues that can enter the cell and be incorporated into the CoQ10 synthesis pathway downstream of the affected enzyme, examples being 4-hydroxybenzoic acid, 2,4-dihydroxybenzoic acid or vanillic acid, which, in contrast to CoQ10, are small, water-soluble molecules. In this article, we have, therefore, reviewed potential bypass mechanisms for primary CoQ10 deficiencies, PDSS1, PDSS2 to COQ10, together with NDUFA9 and HPDL, using such precursors. Most of the published data relating to the bypass therapy of primary CoQ10 deficiency is derived from cell lines or animal models, and few human studies have so far been undertaken. In addition, further research is required to investigate the potential mechanisms by which bypass compounds such as 4-HB may access the human blood-brain barrier (BBB), for example, using in vitro co-culture BBB model systems incorporating CoQ10-deficient neurons. Overall, the objective of this article is, therefore, to systematically review the available data for each of the primary CoQ10 deficiencies, PDSS1, PDSS2 to COQ10 together with NDUFA9 and HPDL, in particular to identify the clinical potential of such studies. - Source: PubMed
Publication date: 2026/04/15
Mantle DavidCufflin NeveHargreaves Iain P - The role of 4-hydroxyphenylpyruvate dioxygenase-like protein (HPDL) in endometrial cancer (EC) progression remains poorly understood, particularly its involvement in metabolic-epigenetic crosstalk via lactate-driven histone lactylation. This study aimed to investigate HPDL's mechanistic contribution to EC pathogenesis. - Source: PubMed
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Wang YanZhu JialeiWei ShiyangJin LijieLiu ZhanqiuXu JieYang NanaJiang XuefengWang CaizhiWang Lingling - This study systematically investigates the laser surface hardening (LSH) behavior of two medium carbon steels-the low alloy 42CrMo4 and the plain carbon C45-using a 4 kW high power diode laser (HPDL). The influence of laser parameters (power: 3.0-3.8 kW; scanning speed: 10-16 mm/s), post-laser quenching medium (oil vs. air), and, critically, the initial material condition (normalized "raw" vs. quenched and tempered "Q&T") on the case hardening depth (CHD) was evaluated. Hardness profiles defined the CHD at a threshold of 392 HV1, and microstructural analysis was conducted via optical microscopy. The results demonstrate that prior conventional Q&T heat treatment of 42CrMo4 enhances the subsequent laser-hardened depth by approximately 27% compared to laser treatment of the normalized material under identical parameters, providing a quantitative basis for process optimization. For Q&T 42CrMo4, the quenching medium had an insignificant effect on CHD, with air cooling proving equally effective as oil across the tested parameter range, offering an empirically validated route for sustainable processing. In contrast, C45 exhibited a substantially lower and less parameter-sensitive CHD, constrained by its inherent low hardenability. This comparative analysis underscores that hardening depth in 42CrMo4 is linearly controllable via energy input, whereas for C45 it is hardenability-limited. This work establishes that an integrated approach combining conventional bulk heat treatment with diode laser hardening using air cooling offers a highly effective, controllable, and sustainable surface engineering route for high-performance alloy steels. - Source: PubMed
Publication date: 2026/03/03
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