Cleaver Scientific Ampholytes 3-10 Iso-Dalt
- Known as:
- Cleaver Scientific Ampholytes 3-10 Iso-Dalt
- Catalog number:
- CSL-AMP3-10/2ID
- Product Quantity:
- x 2
- Category:
- -
- Supplier:
- Cleaver
- Gene target:
- Cleaver Scientific Ampholytes 3-10 Iso-Dalt
Related genes to: Cleaver Scientific Ampholytes 3-10 Iso-Dalt
- Gene:
- ACSM6 NIH gene
- Name:
- acyl-CoA synthetase medium chain family member 6
- Previous symbol:
- C10orf129
- Synonyms:
- bA310E22.3
- Chromosome:
- 10q23.33
- Locus Type:
- gene with protein product
- Date approved:
- 2004-05-27
- Date modifiied:
- 2017-06-13
- Gene:
- AGBL1 NIH gene
- Name:
- ATP/GTP binding protein like 1
- Previous symbol:
- -
- Synonyms:
- FLJ32310, CCP4
- Chromosome:
- 15q25.3
- Locus Type:
- gene with protein product
- Date approved:
- 2004-11-19
- Date modifiied:
- 2017-05-11
- Gene:
- ANTXR2 NIH gene
- Name:
- ANTXR cell adhesion molecule 2
- Previous symbol:
- -
- Synonyms:
- CMG2, CMG-2, FLJ31074
- Chromosome:
- 4q21.21
- Locus Type:
- gene with protein product
- Date approved:
- 2003-09-25
- Date modifiied:
- 2018-05-10
- Gene:
- C1QTNF3 NIH gene
- Name:
- C1q and TNF related 3
- Previous symbol:
- -
- Synonyms:
- CTRP3, Cors, Corcs, 2310005P21Rik, Cors-26
- Chromosome:
- 5p13.2
- Locus Type:
- gene with protein product
- Date approved:
- 2001-10-02
- Date modifiied:
- 2017-03-01
- Gene:
- C18orf21 NIH gene
- Name:
- chromosome 18 open reading frame 21
- Previous symbol:
- -
- Synonyms:
- PNAS-131, PNAS-124, HsT3108
- Chromosome:
- 18q12.2
- Locus Type:
- gene with protein product
- Date approved:
- 2004-05-05
- Date modifiied:
- 2016-09-30
Related products to: Cleaver Scientific Ampholytes 3-10 Iso-Dalt
(+/-)-Iso Myosmine , Technical Grade CAS: 53844-46-5 Formula: C9H10N2 (+_-)-Iso Myosmine , Technical Grade C9H10N2 CAS: 53844-46-5 (R) 1_(1_Napthyl) Ethyl Iso Cyanate (R) 1_(1_Napthyl) Ethyl I(R)_(+)_3_(Acetylthio)isobutyric acid meth (R)_(+)_3_(Acetylthio)iso(R,S)-Iso Valganciclovir C14H22N6O5 CAS:(R,S)-Iso Valganciclovir CAS: Formula: C14H22N6O5(S)-Naproxen Iso-acyl-β-D-glucuronide
DISCONTINUED C20H22O9 CAS: 219476-92-3 (S)-Naproxen Iso-acyl-β-D-glucuronide
DISCONTINUED CAS: 219476-92-3 Formula: C20H22O9 (S)_(_)_3_(Acetylthio)isobutyricAcid (S)_(_)_3_(Acetylthio)iso(S,R)-Iso Valganciclovir C14H22N6O5 CAS:(S,R)-Iso Valganciclovir CAS: Formula: C14H22N6O51 4" ISO to 1 8" Tubing Adapter1,1,1_trihydroxyethyl isocyanate 1,1,1_trihydroxyethyl iso1,1,4,4_tetramethylbutane_1,4_diyl bis(iso 1,1,4,4_tetramethylbuta1,1,5_trimethylheptyl isobutyrate 1,1,5_trimethylheptyl iso Related articles to: Cleaver Scientific Ampholytes 3-10 Iso-Dalt
- Esophageal Cancer (EC) ranks among the most common malignancies worldwide. Most EC patients acquire drug resistance to chemotherapy either intrinsically or acquired after T-DM1 treatment, which shows that increasing or decreasing the expression of particular genes might influence chemotherapeutic sensitivity or resistance. Therefore, gaining a deeper understanding of the altered expression of genes involved in EC drug resistance and developing new therapeutic methods are essential targets for continued advancement in EC therapy. - Source: PubMed
Publication date: 2024/09/06
Yazdani FatemeMottaghi-Dastjerdi NegarShahbazi BehzadAhmadi KhadijehGhorbani AbozarSoltany-Rezaee-Rad MohammadMontazeri HamedKhoshdel FarzaneGuzzi Pietro Hiram - Interleukin (IL)-33 is a cytokine that appears to mediate fibrosis by signaling via its receptor ST2 (IL-33R/IL1RL1). It is also, however, a protein that after synthesis is sorted to the cell nucleus, where it appears to affect chromatin folding. Here we describe a novel role for nuclear IL-33 in regulating the fibroblast phenotype in murine kidney fibrosis driven by unilateral ureteral obstruction. Transcriptional profiling of IL-33-deficient kidneys 24 h after ligation revealed enhanced expression of fibrogenic genes and enrichment of gene sets involved in extracellular matrix formation and remodeling. These changes relied on intracellular effects of IL-33, because they were not reproduced by treatment with a neutralizing antibody to IL-33 that prevents IL-33R/ST2L receptor signaling nor were they observed in IL-33R/ST2-deficient kidneys. To further explore the intracellular function of IL-33, we established transcription profiles of human fibroblasts, observing that knockdown of IL-33 skewed the transcription profile from an inflammatory towards a myofibroblast phenotype, reflected in higher levels of COL3A1, COL5A1 and transgelin protein, as well as lower expression levels of IL6, CXCL8, CLL7 and CCL8. In conclusion, our findings suggest that nuclear IL-33 in fibroblasts dampens the initial profibrotic response until persistent stimuli, as enforced by UUO, can override this protective mechanism. - Source: PubMed
Publication date: 2021/01/08
Gatti FrancescaMia SobujHammarström ClaraFrerker NadineFosby BjarteWang JunbaiPietka WojciechSundnes OlavHol JohannaKasprzycka MonikaHaraldsen Guttorm - To investigate differential genes (DEGs) between no/mild and severe emphysema by bioinformatics analysis. The microarray dataset GSE1650, of lung tissue in no/mild and severe emphysema, was downloaded from the GEO database, and DEGs were obtained by test. Analysis of DEGs based on DAVID database was used to obtain gene ontology (GO) and kyoto encyclopedia of genes and genomes (KEGG) pathway. The protein-protein interaction network (PPI) was established using STRING database to identify hub genes. A total of 76 DEGs were obtained, of which 62 genes were up-regulated and 14 genes were down-regulated in severe emphysema group. Gene ontology showed that the DEGs were mainly involved in neutrophil chemotaxis, cellular response to interleukin-1, extracellular matrix organization, immune response, and KEGG pathway involved cytokine-cytokine receptor interaction, ECM-receptor interaction, PI3K-Akt signaling pathway, platelet activation. Seventeen hub genes were recognized by PPI analysis, including CXCL8, RRAD, CLU, TIMP1, SEPP1, ISLR, BGN, COL1A1, COLIA2, ACTA2, ACTN1, FIGF, TPM1, TPM2, LUM, COL6A3 and TAGLN. Among them, fifteen genes (CLU, TIMP1, SEPP1, ISLR, BGN, COLIA2, COL1A1, ACTA2, ACTN1, FIGF, TPM1, TPM2, LUM, COL6A3, TAGLN) were up-regulated and two genes (CXCL8, RRAD) were down-regulated. Bioinformatics analysis based on GEO database showed that there were DEGs between non/mild and severe emphysema patients. - Source: PubMed
Qin J YJia H ZZhang YLi D DShen Y CChen LWen F Q - Although therapies with human amnion/chorion are used to ameliorate acute and chronic wounds, it is unclear which component of the amnion/chorion tissue promotes wound healing. To characterize the comparative effects of amnion and chorion in wound healing, we used human adipose-derived stromal cells to assess cell viability, migration, and gel contraction after treatment with amnion membrane extract (AME) or chorion membrane extract (CME). We then correlated the possible effectors via AME and CME protein profiling, and compared them by enzyme-linked immunosorbent assay (ELISA), western blotting, and immunocytochemistry. Cell viability was significantly increased with 50 and 100 μg/mL AME treatment, but with CME treatment, a significant increase was only observed with 100 μg/mL. With CME treatment, cell migration was 2.22-fold greater than the control, and collagen gels showed 20% greater contraction. Compared to control, the expression levels of α-smooth muscle actin (SMA) and smooth muscle protein 22-alpha (SM22α) increased both with AME and CME treatments, whereas calponin expression decreased. Protein profiling revealed significantly higher tissue inhibitor of metalloproteinase-1 (TIMP-1), interleukin-8, exotoxin, and adiponectin levels in CME than in AME, and ELISA revealed 8-fold higher adiponectin levels in cells treated with CME than those treated with AME. Immunocytochemistry revealed that α-SMA, SM22α, and calponin were significantly higher in CME- than AME-treated cells; however, adiponectin treatment did not enhance α-SMA, SM22α, or calponin expression. In conclusion, amnion and chorion membrane extracts exerted differential effects on proliferation and contraction of human adipose-derived stromal cells. Amnion extract was superior at inducing cell proliferation and migration, whereas CME was superior at inducing cell contraction. - Source: PubMed
Namgoong SikLee HyunsuLee Jae-SunJeong Seong HoHan Seung-KyuDhong Eun-Sang