MOUSE STOMACH TOTAL PROTEIN LYSATE (0 DAY OLD)
- Known as:
- MOUSE STOMACH TOTAL PROTEIN LYSATE (0 DAY OLD)
- Catalog number:
- ABS10243
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- AbD
- Gene target:
- MOUSE STOMACH TOTAL PROTEIN LYSATE (0 DAY OLD)
Related genes to: MOUSE STOMACH TOTAL PROTEIN LYSATE (0 DAY OLD)
- Gene:
- KCTD13 NIH gene
- Name:
- potassium channel tetramerization domain containing 13
- Previous symbol:
- -
- Synonyms:
- PDIP1, FKSG86, POLDIP1
- Chromosome:
- 16p11.2
- Locus Type:
- gene with protein product
- Date approved:
- 2003-11-24
- Date modifiied:
- 2014-11-19
- Gene:
- PNPT1 NIH gene
- Name:
- polyribonucleotide nucleotidyltransferase 1
- Previous symbol:
- DFNB70
- Synonyms:
- PNPase, OLD35, old-35
- Chromosome:
- 2p16.1
- Locus Type:
- gene with protein product
- Date approved:
- 2003-09-25
- Date modifiied:
- 2016-10-05
- Gene:
- POLD1 NIH gene
- Name:
- DNA polymerase delta 1, catalytic subunit
- Previous symbol:
- POLD
- Synonyms:
- CDC2
- Chromosome:
- 19q13.3
- Locus Type:
- gene with protein product
- Date approved:
- 1992-02-06
- Date modifiied:
- 2019-04-23
- Gene:
- POLD4 NIH gene
- Name:
- DNA polymerase delta 4, accessory subunit
- Previous symbol:
- -
- Synonyms:
- p12, POLDS
- Chromosome:
- 11q13.2
- Locus Type:
- gene with protein product
- Date approved:
- 2000-12-04
- Date modifiied:
- 2016-10-05
- Gene:
- TYRP1 NIH gene
- Name:
- tyrosinase related protein 1
- Previous symbol:
- TYRP, CAS2
- Synonyms:
- GP75, CATB, TRP, b-PROTEIN, OCA3
- Chromosome:
- 9p23
- Locus Type:
- gene with protein product
- Date approved:
- 1991-09-04
- Date modifiied:
- 2016-04-19
Related products to: MOUSE STOMACH TOTAL PROTEIN LYSATE (0 DAY OLD)
Related articles to: MOUSE STOMACH TOTAL PROTEIN LYSATE (0 DAY OLD)
- The evolution of personalized medicine in dermatology signifies a transformative shift towards individualized treatments, driven by the integration of biomarkers. These molecular indicators serve beyond diagnostics, offering insights into disease staging, prognosis, and therapeutic monitoring. Specific criteria guide biomarker selection, ensuring attributes like specificity, sensitivity, cost feasibility, stability, rapid detection, and reproducibility. This literature review, based on data from PubMed, SCOPUS, and Web of Science, explores biomarkers in Hidradenitis Suppurativa (HS), Psoriasis, Atopic Dermatitis (AD), Alopecia Areata (AA), Vitiligo, and Chronic Spontaneous Urticaria (CSU). In HS, TNF-α, IL-1β, and MMPs serve as biomarkers, influencing targeted therapies like adalimumab and anakinra. Psoriasis involves biomarkers such as TNF-α, IL-23, and HLA genes, shaping treatments like IL23 and IL17 inhibitors. AD biomarkers include ECP, IL-4, IL-13, guiding therapies like dupilumab and tralokinumab. For AA, lipocalin-2, cytokines, and genetic polymorphisms inform JAK inhibitors' use. Vitiligo biomarkers range from cytokines to genetic markers like TYR, TYRP1, guiding treatments like JAK inhibitors. CSU biomarkers encompass IgE, cytokines, and autologous serum tests, influencing therapies like omalizumab and cyclosporine. Comparing conditions, common proinflammatory markers reveal limited specificity. While some biomarkers aid diagnosis and standard treatments, others hold more scientific than clinical value. Precision medicine, driven by biomarkers, has shown success in skin malignancies. Future directions involve AI-powered algorithms, nanotechnology, and multi-omics integration for personalized dermatological care. - Source: PubMed
Publication date: 2024/03/30
Tan Isabella JPodwojniak AliciaParikh AarushiCohen Bernard A - Exploration of gene expression variations is a potential source to unravel biological pathways involved in pathological changes in body and understand the mechanism underneath. Vitiligo patients were explored for gene expression changes transcriptionally at perilesional site in comparison to normal site of same patients for melanogenesis pathway (TYR, DCT & TYRP1) cell adhesion (MMPs & TIMP1), cell survival (BCL2 & BAX1) as well as proliferation, migration & development (SOX9, SOX10 & MITF) regulatory system, using skin biopsy samples. Results were also compared with changes in gene expression for melanocytes under stress after hydrogen peroxide treatment in-vitro. Gene amplification was carried out via real time PCR. We found increased expression of proliferation, migration & development regulatory genes as well as melanogenesis pathway genes at perilesional site of patients. In-vitro study also supports induced MITF expression and disturbed melanogenesis in melanocytes under stress. Expression level ratio of cell survival regulatory genes' (BCL2/BAX1) as well as cell adhesion regulatory genes (MMPs/TIMP1) was observed upregulated at patient's perilesional site however downregulated in hydrogen peroxide treated melanocytes in-vitro. Observed upregulated gene expression at perilesional site of patients may be via positive feedback loop in response to stress to increase cell tolerance power to survive against adverse conditions. Gene expression analysis suggests better cell survival and proliferation potential at perilesional site in vitiligo patients. It seems in-vivo conditions/growth factors supports cells to fight for survival to accommodate stressed conditions. - Source: PubMed
Publication date: 2024/04/25
Tanwar SushmaParsad Davinder - Melanin is the major pigment responsible for the coloring of mammalian skin, hair, and eyes to defend against ultraviolet radiation. However, excessive melanin production has resulted in numerous types of hyperpigmentation disorders. Tyrosinase-related protein 1 (TYRP1) is a transmembrane glycoprotein enzyme found in many organisms, including humans, that plays an important role in melanogenesis. Thus, controlling the enzyme activity of TYRP1 with tyrosinase inhibitors is a vital step in the treatment of hyperpigmentation problems in humans. In the present investigation, virtual screening, pharmacokinetics, drug docking, and molecular dynamics (MD) simulation were used to find the most potent drug as an inhibitor of TYRP1 to effectively treat hyperpigmentation disorder. The 3D structure of TYRP1 was retrieved from the Protein Data Bank (PDB) database (PDB ID: 5M8M) and validated by the Ramachandran plot. Pharmacokinetics and drug-likeness showed that mycosporine 2 glycine (M2G) and shinorine (SHI) were the best compounds over other ligands in the same (P-1) structural pose. However, MD simulations of the M2G showed the highest CDOCKER interaction energy (-45.182 kcal/mol) and binding affinity (-65.0529 kcal/mol) as compared to SHI and reference drugs. The molecular binding modes RMSD and RMSF plots have exhibited more relevance to the M2G ligand in comparison to other drug ligands. The bioactivity and ligand efficiency profiles revealed that M2G is the most effective compound as a TYRP1 inhibitor. Thus, M2G could be used as a most effective drug for developing valuable sunscreen products to cure hyperpigmentation-related diseases. - Source: PubMed
Publication date: 2024/04/23
Amin NasreenSingh Vinay KKannaujiya Vinod K - Bioassay and HPLC-UV guided fractionations of the crude extract of marine-derived sp. SNA-077 have led to the isolation of a red pigment, undecylprodigiosin . The chemical structure of undecylprodigiosin was revealed by the interpretation of NMR and mass spectroscopic (MS) data. Further, anti-melanogenic effects of undecylprodigiosin were investigated. First, the melanin contents of undecylprodigiosin -treated B16 cells were evaluated. Furthermore, undecylprodigiosin significantly inhibited the key enzymes involved in melanogenesis, including tyrosinase, tyrosinase related protein-1 (TYRP-1), and dopachrome tautomerase (DCT). The mRNA and protein expression levels of Microphthalmia-associated transcriptian factor (MiTF), a critical transcription factor for tyrosinase gene expression, were also suppressed by undecylprodigiosin treatment in B16 analyses. Collectively, our results suggest for the first time that undecylprodigiosin , a potent component isolated from an extract of marine sp. SNA-077, critically exerts the anti-melanogenic ability for melanin synthesis. - Source: PubMed
Publication date: 2024/04/23
Lee ChaeyoungPark Jung MinHillman Prima FYoo MinyiKim Hye YeonLee Chang-SeokNam Sang-Jip - The pigmentation of the skin, modulated by different actors in melanogenesis, is mainly due to the melanins (protective pigments). In humans, these pigments' precursors are synthetized by an enzyme known as tyrosinase (TyH). The regulation of the enzyme activity by specific modulators (inhibitors or activators) can offer a means to fight hypo- and hyper-pigmentations responsible for medical, psychological and societal handicaps. Herein, we report the investigation of phenylalanine derivatives as TyH modulators. Interacting with the binuclear copper active site of the enzyme, phenylalanine derivatives combine effects induced by combination with known resorcinol inhibitors and natural substrate/intermediate (amino acid part). Computational studies including docking, molecular dynamics and free energy calculations combined with biological activity assays on isolated TyH and in human melanoma MNT-1 cells, and X-ray crystallography analyses with the TyH analogue Tyrp1, provide conclusive evidence of the interactions of phenylalanine derivatives with human tyrosinase. In particular, our findings indicate that an analogue of L-DOPA, namely (S)-3-amino-tyrosine, stands out as an amino phenol derivative with inhibitory properties against TyH. - Source: PubMed
Publication date: 2024/04/20
Faure ClarisseNg Yi MingBelle CatherineSoler-Lopez MontserratKhettabi LynaSaidi MelissaBerthet NathalieMaresca MarcPhilouze ChristianRachidi WalidReglier Mariusdu Moullinet d'Hardemare AmauryJamet Hélène