GATA4 (P101) pAb host: Rabbit
- Known as:
- GATA4 (P101) pAb production species: Rabbit
- Catalog number:
- bs1747
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Bioworld
- Gene target:
- GATA4 (P101) pAb host: Rabbit
Related genes to: GATA4 (P101) pAb host: Rabbit
- 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:
- PPP1R18 NIH gene
- Name:
- protein phosphatase 1 regulatory subunit 18
- Previous symbol:
- KIAA1949
- Synonyms:
- phostensin
- Chromosome:
- 6p21.33
- Locus Type:
- gene with protein product
- Date approved:
- 2004-03-02
- Date modifiied:
- 2016-10-05
Related products to: GATA4 (P101) pAb host: Rabbit
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
- Spinal cord injury in mammals triggers fibrotic scar formation that impedes axon regrowth, whereas zebrafish regenerate and recover motor function without persistent fibrosis. Here, we identify the transcription factor Gata4 as a regulator of regeneration-associated extracellular matrix (ECM) remodeling. Following injury, gata4 is induced predominantly in ependymo-radial glial cells (ERGs). Gata4 preserves ERG identity and suppresses a fibroblast-like transcriptional program enriched for ECM genes. Loss of Gata4 increases expression of the collagen cross-linking enzyme Loxl2b, resulting in excessive collagen cross-linking, matrix stiffening, and a regeneration-inhibitory ECM environment. These changes delay glial and axonal bridging and impair motor recovery. Pharmacological inhibition of Loxl2b rescues ECM organization, tissue bridging, and functional recovery. Injury-induced gata4 expression depends in part on Hif-1α signaling and activation of an injury-responsive cis-regulatory element. Together, these findings identify a Gata4-Loxl2b axis linking glial cell state to ECM mechanics during spinal cord regeneration. - Source: PubMed
Publication date: 2026/10/05
Noel Nicolas PLima Fernandes Vânia FKjar AndrewPfotenhauer Paige EKim HyosungSefogbe Mawusi PAkam-Baxter Eman ALippmann Ethan SCigliola Valentina - Human pluripotent stem cell-derived cardiomyocytes (hPSC-CMs) hold tremendous promise for disease modeling, drug discovery, and cardiac regenerative therapies. However, the immature phenotype of hPSC-CMs remains a major barrier limiting their translational utility. Here, we performed integrated multi-omic profiling to identify molecular pathways and regulatory programs associated with hPSC-CM maturation during long-term culture. hPSC-CMs were cultured for 113 days and analyzed using metabolomics, proteomics, and transcriptomics across progressive stages of maturation. Long-term culture induced widespread multi-omic remodeling, including significant changes in 142/934 metabolites, 550/3556 proteins, and 2892/23,309 transcripts from Day 30 to Day 113. Metabolomic analyses revealed early increases in phospholipid biosynthesis and mitochondrial beta oxidation of fatty acids from Day 30 to Day 60, suggesting metabolic priming precedes later maturation events. In contrast, proteomic remodeling was more prominent during later stages of maturation and was characterized by enhanced calcium handling and cell cycle exit. Transcriptomic analyses demonstrated progressive increases in ion channel expression, t-tubule organization, fatty acid metabolism, creatine shuttle pathways, and cell cycle arrest programs. Transcriptomic and integrative multi-omic pathway analyses identified coordinated suppression of TGFβ, MAPK, Wnt, and Hedgehog signaling together with activation of integrin-related, respiratory electron transport, muscle contraction, and Slit-Robo signaling pathways during maturation. Moreover, multi-omic transcription factor activity analysis prioritized a GATA4-centered network of putative cardiomyocyte maturation regulators including SOX7, SOX18, TBX2, and ZFPM2 (FOG2). Together, these findings elucidate the degree and pace of hPSC-CM maturation during long-term culture and establish an integrated multi-omic framework for identifying strategies to accelerate hPSC-CM maturation. - Source: PubMed
Publication date: 2026/10/02
Feeney Austin KSimmons Aaron DBayne Elizabeth FZhu YanlongPark ChanhyungPeplinski Claire JShabnam FathimaZhang XiaotianZhang JianhuaPergande Melissa RKamp Timothy JGe YingPalecek Sean P - Fibroblast migration contributes to the spatial organization of tissue repair and extracellular matrix remodeling, but the transcriptional mechanisms regulating this process under physiologically relevant mechanical conditions remain incompletely understood. We investigated whether GATA4 regulates fibroblast migration in a tissue-of-origin-dependent manner. Cardiac fibroblasts (CFs), lung fibroblasts (LFs), and tail-tip fibroblasts (TTFs) were isolated from neonatal male and female mice and cultured on 8-kPa polydimethylsiloxane substrates. CF behavior on 8-kPa substrates was first compared with that on conventional tissue-culture plastic. was subsequently deleted by adenoviral Cre transduction, and multiple features of steady-state migration were quantified by live-cell imaging. CFs cultured on 8-kPa substrates exhibited a smaller cell area and greater migration speed, displacement, and directional persistence than cells cultured on plastic, establishing a physiologically relevant mechanical baseline. Baseline expression was highest in CFs, intermediate in LFs, and lowest in TTFs, whereas adenoviral Cre reduced expression by more than 90% in all three populations. deletion produced distinct migratory responses according to fibroblast source. In CFs, loss reduced instantaneous speed, line speed, segment length, and directional persistence while increasing cell area. LFs showed modest increases in instantaneous speed, path speed, normalized 1-h path distance, and segment length without a clear change in directional persistence, whereas TTF migration was comparatively insensitive to loss. Integrated effect-size analysis confirmed that the coordinated alteration of migration rate and directionality was most pronounced in CFs. RNA-seq analysis of adult CFs further showed enrichment of general motility and actin-remodeling programs following deletion, without coordinated enrichment of lamellipodium and focal-adhesion programs. Together, these findings indicate that GATA4 supports efficient and persistent fibroblast migration in a fibroblast-source-dependent manner under physiologically relevant mechanical conditions. - Source: PubMed
Publication date: 2026/09/16
Zhang ZhentaoZih-Shuo Jethro WangChen PengXu YanpingYan ZhiyuZhang QingningWang XiAlizai UsmanIkeda TakahideWhitson Bryan APawlik Timothy MZhu Hua - Hypospadias is a common disorder of sex development (DSD), resulting from the impaired formation of the penile urethra. In mammals, penile urethral development depends on androgens secreted during a limited time window immediately after the onset of testis development. In this study, we performed morphological and immunohistochemical analyses of a 15-day-old genetically XY Holstein calf with perineal hypospadias to characterize a unique phenotype providing critical insights into its pathogenic mechanisms. Although the penis and prostate were grossly developed, the penile urethra was not formed. Furthermore, the right testis presented as a streak gonad attached to the dorsal abdominal wall and was covered by a fibrous membrane. Extensive fatty infiltration and a lack of interstitial Leydig cells were observed throughout the testis; however, a few testicular cords containing GATA4/SOX9-positive Sertoli cells and VASA-positive germ cells were identified. In contrast, the left testis was morphologically normal, but exhibited increased expression of the androgen-biosynthetic enzyme P450C17, suggesting compensatory up-regulation of androgen production. These findings suggest that a transient androgen deficiency, caused by developmental arrest of the right testis after testicular cord formation, led to the failure of penile urethral formation. This case provides clinical evidence that the precise timing of unilateral testicular impairment is a critical determinant of the hypospadias phenotype in cattle. - Source: PubMed
Publication date: 2026/10/01
Kajimoto TatsukiSakai KeikoKuroki ChieKobayashi KumiKanai YoshiakiraYanagida AyakaHiramatsu Ryuji - : In situ reprogramming of cardiac fibroblasts into induced cardiomyocytes (iCMs) holds great promise for myocardial infarction (MI) therapy by replenishing lost cardiomyocytes. A transcription factor cocktail consisting of Mef2c, Gata4, and Tbx5 (MGT) represents a widely used starting regimen for cardiac reprogramming, with numerous optimization efforts focused primarily on improving reprogramming efficiency. However, the effects of MGT exposure on non-target cardiac cell populations remain largely uncharacterized, and it remains unclear whether such unintended effects could pose safety concerns. : In this study, we introduced the widely used MGT cocktail into primary mouse bone marrow-derived macrophages (BMDMs) and the immortalized mouse macrophage cell line RAW 264.7. We first assessed cardiomyocyte-associated gene and protein expression. We then examined the polarization state of transduced RAW 264.7 cells. In BMDMs, we further assessed apoptosis- and necroptosis-associated markers to determine whether MGT delivery was accompanied by cell death. : (a) MGT introduction induced a transient increase in cardiomyocyte-associated Tnnt2/Myh6 transcripts and modest cTnT protein induction in macrophages, with cTnT immunofluorescence remaining elevated after two weeks in BMDMs and a small subset of cells displaying fibroblast-like morphology reminiscent of iCMs. (b) Transduced RAW 264.7 cells displayed elevated Cd206 transcript levels, accompanied by an increased proportion of spindle-like cells and enlarged nuclear area, collectively supporting an M2-like polarization shift. (c) Transduced primary BMDMs, but not RAW 264.7 cells, displayed elevated apoptosis- and necroptosis-associated responses, including increased YP1 fluorescence, PI staining, and p-MLKL immunofluorescence. : The classical MGT reprogramming regimen polarized RAW 264.7 cells toward an M2-like state, raising the possibility that, in the TGF-β-rich post-MI environment, this shift could increase the pool of macrophages susceptible to macrophage-to-myofibroblast transition and thereby potentially promote fibrosis. MGT-expressing LV elicited apoptosis-associated and necroptosis-associated changes in transduced BMDMs. These polarization and cell-survival effects highlight potential off-target and safety concerns for in situ direct cardiac reprogramming. Further investigations are warranted to determine whether and how such macrophage perturbations affect tissue remodeling and therapeutic outcomes in the post-MI setting. - Source: PubMed
Publication date: 2026/09/16
Chen TingzhenDing ShanshanZhang ZhongwenZhao LinCao KejunZhang GuannanWeng ChangyaGong GuangyuanXu LiangYang MinLi TianquanSheng ChengyuLi Yanxiu