GATA4 (P101) pAb Host Rabbit Reactivity H,M,R Application WB IHC IF
- Known as:
- GATA4 (P101) pAb Host Rabbit Reactivity H,M,R Application Western Blot Immunohistochemistry IF
- Catalog number:
- BS1747
- Product Quantity:
- 100ug
- Category:
- -
- Supplier:
- Bioword
- Gene target:
- GATA4 (P101) pAb Host Rabbit Reactivity Application IHC
Related genes to: GATA4 (P101) pAb Host Rabbit Reactivity H,M,R Application WB IHC IF
- Gene:
- DKC1 NIH gene
- Name:
- dyskerin pseudouridine synthase 1
- Previous symbol:
- DKC
- Synonyms:
- XAP101, dyskerin, NAP57, NOLA4, Cbf5
- Chromosome:
- Xq28
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-22
- Date modifiied:
- 2019-04-23
- Gene:
- GATA4 NIH gene
- Name:
- GATA binding protein 4
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 8p23.1
- Locus Type:
- gene with protein product
- Date approved:
- 1994-11-30
- Date modifiied:
- 2016-10-05
- Gene:
- LRATD2 NIH gene
- Name:
- LRAT domain containing 2
- Previous symbol:
- FAM84B
- Synonyms:
- BCMP101, NSE2
- Chromosome:
- 8q24.21
- Locus Type:
- gene with protein product
- Date approved:
- 2005-07-28
- Date modifiied:
- 2019-03-01
- Gene:
- PIK3R5 NIH gene
- Name:
- phosphoinositide-3-kinase regulatory subunit 5
- Previous symbol:
- -
- Synonyms:
- P101-PI3K, p101
- Chromosome:
- 17p13.1
- Locus Type:
- gene with protein product
- Date approved:
- 2004-10-13
- Date modifiied:
- 2015-11-17
- Gene:
- RNVU1-18 NIH gene
- Name:
- RNA, variant U1 small nuclear 18
- Previous symbol:
- RNU1P1, RNU1-5, RNU1-25, RNU1-25P
- Synonyms:
- vU1.18, U1P101, U1P15, U1.15
- Chromosome:
- 1q21.2
- Locus Type:
- RNA, small nuclear
- Date approved:
- 2009-11-05
- Date modifiied:
- 2014-11-18
Related products to: GATA4 (P101) pAb Host Rabbit Reactivity H,M,R Application WB IHC IF
guanine nucleotide binding protein alpha inhibiting activity polypeptide 1 (GNAI1) polyclonal antibody kinase suppressor of ras (KSR) polyclonal antibody'F 4_80 Antigen (mouse) Host Rat'F 4_80 Antigen (mouse) Host Rat(Alpha)_ 1 _ antitrypsin (A1AT) POLYCLONAL Rabbit anti_human(Alpha)_ Feto Protein (AFP) POLYCLONAL Rabbit anti_human(Alpha)_ Feto Protein (AFP) POLYCLONAL Rabbit anti_human(Alpha)_1_ antitrypsin (A1AT) POLYCLONAL Rabbit anti_human(Arg6,b_cyclohexyl_Ala8,D_Tic16,Arg17,Cys18)_Atrial Natriuretic Factor (6_18) amide (mouse, rabbit, rat) Salt _ Binding (Disulfide_bond) Synonym A71915 SumFormula C69H116N26O15S2(Arg6,b_cyclohexyl_Ala8,D_Tic16,Arg17,Cys18)_Atrial Natriuretic Factor (6_18) amide (mouse, rabbit, rat) Salt _ Binding (Disulfide_bond) Synonym A71915 SumFormula C69H116N26O15S2(Arg6,β-cyclohexyl-Ala8,D-Tic16,Arg17,Cys18)-Atrial Natriuretic Factor (6-18) amide (mouse, rabbit, rat)
A71915 98% C69H116N26O15S2 CAS:(Arg8)-Vasopressin - Diluted Antiserum for RIA, Host Guinea Pig(Arg8)-Vasopressin - Diluted Antiserum for RIA, Host Rabbit(Arg8)-Vasopressin - Diluted Antiserum for RIA, Host: Guinea Pig(Arg8)-Vasopressin - Diluted Antiserum for RIA, Host: Guinea Pig Related articles to: GATA4 (P101) pAb Host Rabbit Reactivity H,M,R Application WB IHC IF
- The ability to generate functional hepatocytes without relying on donor liver organs holds significant therapeutic promise in the fields of regenerative medicine and potential liver disease treatments. Clustered regularly interspaced short palindromic repeats (CRISPR) activator (CRISPRa) is a powerful tool that can conveniently and efficiently activate the expression of multiple endogenous genes simultaneously, providing a new strategy for cell fate determination. The main purpose of this study is to explore the feasibility of applying CRISPRa for hepatocyte reprogramming and its application in the treatment of mouse liver fibrosis. - Source: PubMed
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Publication date: 2023/12/06
Ramgir Shalaka SAnnamalai SivakumarAbilash V G - In mammals, gonadal somatic cell lineage differentiation determines the development of the bipotential gonad into either the ovary or testis. Sertoli cells, the only somatic cells in the spermatogenic tubules, support spermatogenesis during gonadal development. During embryonic Sertoli cell lineage differentiation, relevant genes, including , , , , , , , and , are expressed at specific times and in specific locations to ensure the correct differentiation of the embryo toward the male phenotype. The dysregulated development of Sertoli cells leads to gonadal malformations and male fertility disorders. Nevertheless, the molecular pathways underlying the embryonic origin of Sertoli cells remain elusive. By reviewing recent advances in research on embryonic Sertoli cell genesis and its key regulators, this review provides novel insights into sex determination in male mammals as well as the molecular mechanisms underlying the genealogical differentiation of Sertoli cells in the male reproductive ridge. - Source: PubMed
Publication date: 2024/04/18
Gao YangWang ZicanLong YueYang LiciJiang YongjianDing DongyuTeng BaojianChen MinYuan JinxiangGao Fei - Liver sinusoidal endothelial cells (LSECs) are important in liver development, regeneration, and pathophysiology, but the differentiation process underlying their tissue-specific phenotype is poorly understood and difficult to study because primary human cells are scarce. The aim of this study was to use human induced pluripotent stem cell (hiPSC)-derived LSEC-like cells to investigate the differentiation process of LSECs. - Source: PubMed
Publication date: 2024/02/01
Yap Kiryu KSchröder JanGerrand Yi-WenDobric AleksandarKong Anne MFox Adrian MKnowles BrettBanting Simon WElefanty Andrew GStanley Eduoard GYeoh George CLockwood Glen PCogger Victoria CMorrison Wayne APolo Jose MMitchell Geraldine M - Familial hypertrophic cardiomyopathy (HCM) is a significant precursor of heart failure and sudden cardiac death, primarily caused by mutations in sarcomeric and structural proteins. Despite the extensive research on the HCM genotype, the complex and context-specific nature of many signaling and metabolic pathways linking the HCM genotype to phenotype has hindered therapeutic advancements for patients. Here, we have developed a computational model of HCM encompassing cardiomyocyte signaling and metabolic networks and their associated interactions. Utilizing a stochastic logic-based ODE approach, we linked cardiomyocyte signaling to the metabolic network through a gene regulatory network and post-translational modifications. We validated the model against published data on activities of signaling species in the HCM context and transcriptomes of two HCM mouse models (i.e., R403Q-αMyHC and R92W-TnT). Our model predicts that HCM mutation induces changes in metabolic functions such as ATP synthase deficiency and a transition from fatty acids to carbohydrate metabolism. The model indicated major shifts in glutamine-related metabolism and increased apoptosis after HCM-induced ATP synthase deficiency. We predicted that the transcription factors STAT, SRF, GATA4, TP53, and FoxO are the key regulators of cardiomyocyte hypertrophy and apoptosis in HCM in alignment with experiments. Moreover, we identified shared (e.g., activation of PGC1α by AMPK, and FHL1 by titin) and context-specific mechanisms (e.g., regulation of Ca2+ sensitivity by titin in HCM patients) that may control genotype-to-phenotype transition in HCM across different species or mutations. We also predicted potential combination drug targets for HCM (e.g., mavacamten plus ROS inhibitors) preventing or reversing HCM phenotype (i.e., hypertrophic growth, apoptosis, and metabolic remodeling) in cardiomyocytes. This study provides new insights into mechanisms linking genotype to phenotype in familial hypertrophic cardiomyopathy and offers a framework for assessing new treatments and exploring variations in HCM experimental models. - Source: PubMed
Publication date: 2024/04/24
Khalilimeybodi ASaucerman Jeffrey JRangamani P