Mcl-1 (S155) pAb host: Rabbit
- Known as:
- Mcl-1 (S155) pAb production species: Rabbit
- Catalog number:
- ap0457
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Bioworld
- Gene target:
- Mcl-1 (S155) pAb host: Rabbit
Related genes to: Mcl-1 (S155) pAb host: Rabbit
- Gene:
- AKAP17A NIH gene
- Name:
- A-kinase anchoring protein 17A
- Previous symbol:
- CXYorf3, SFRS17A
- Synonyms:
- XE7, XE7Y, DXYS155E, MGC39904, 721P, CCDC133
- Chromosome:
- Xp22.33 and Yp11.32
- Locus Type:
- gene with protein product
- Date approved:
- 2006-09-22
- Date modifiied:
- 2015-11-17
- Gene:
- CSDE1 NIH gene
- Name:
- cold shock domain containing E1
- Previous symbol:
- -
- Synonyms:
- D1S155E, UNR
- Chromosome:
- 1p13.2
- Locus Type:
- gene with protein product
- Date approved:
- 2005-07-26
- Date modifiied:
- 2016-02-29
- Gene:
- MCL1 NIH gene
- Name:
- MCL1 apoptosis regulator, BCL2 family member
- Previous symbol:
- -
- Synonyms:
- BCL2L3, Mcl-1
- Chromosome:
- 1q21.2
- Locus Type:
- gene with protein product
- Date approved:
- 1993-11-09
- Date modifiied:
- 2019-01-25
- 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
- Gene:
- RNA5SP155 NIH gene
- Name:
- RNA, 5S ribosomal pseudogene 155
- Previous symbol:
- RN5S155
- Synonyms:
- -
- Chromosome:
- 4p16.1
- Locus Type:
- pseudogene
- Date approved:
- 2011-10-10
- Date modifiied:
- 2014-11-19
Related products to: Mcl-1 (S155) 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: Mcl-1 (S155) pAb host: Rabbit
- Huo-Xue-Xiao-Zhong Decoction (HXXZ), a traditional Chinese medicine formulation comprising 14 herbal components, has demonstrated significant efficacy and favorable safety profiles in clinical trials for the prevention of deep vein thrombosis (DVT). However, the underlying molecular mechanisms responsible for its therapeutic effects remain to be elucidated. - Source: PubMed
Publication date: 2026/06/06
Li JizhengYang LijuanWang RongyiLiu YangYe GuoyuWen LichengLong WeibiaoLi FanbingSong En - Efficient differentiation of pluripotent stem cells (PSCs) into functional cells is critical for regenerative medicine and biomanufacturing, yet is often hampered by apoptosis. Ginkgolide A (GA) is a diterpene lactone derived from Ginkgo biloba leaves and a member of the ginkgolide family, compounds known for diverse biological activities including neuroprotection and cardiovascular regulation. However, the mechanism by which ginkgolides influence the directed differentiation of stem cells remains unclear. Here, using a CRISPR-Cas9-engineered TNNT2-mCherry reporter PSC line and a defined cardiac differentiation protocol, we screened ginkgolides for their effects on cardiomyocyte production. Results demonstrated that GA significantly enhanced cardiomyocyte induction efficiency and accelerated the onset of spontaneous beating. Concurrently, GA effectively inhibited apoptosis during differentiation and RNA-seq results also revealed that GA orchestrates stage-specific upregulation of anti-apoptotic genes (e.g., MCL1, XIAP) and core cardiogenic transcription factors (NKX2-5, GATA4). Molecular docking predictions suggested a high binding potential between GA and cytochrome c, suggesting GA might inhibit the intrinsic mitochondrial apoptosis cascade by interfering with cytochrome c's binding to Apoptotic Peptidase Activating Factor-1 (APAF-1). These data demonstrate that GA enhances the differentiation of pluripotent stem cells into cardiomyocytes, potentially through its anti-apoptotic effect. This mechanism highlights its potential as a safe culture additive to boost cell survival and yield for large-scale biomanufacturing and tissue engineering applications. - Source: PubMed
Publication date: 2026/06/05
Xu WenjieWu XiaolongLei ZuoDang XiaoyuShi HongzhaoLi JiannanYuan LimingZhao YayaLi WenhaoChen JingLi NaHua Jinlian - - Source: PubMed
Publication date: 2026/06/05
Karsa MawarKarsa AyuSpurling DaynaXiao LinRonca EmmaBongers AngelikaGao WeimanGifford Andrew JEl-Ayoubi AliCheung Laurence CKotecha Rishi SLock Richard BTeh Charis ELessene GuillaumeNorris Murray DWei AndrewHaber MichelleHenderson Michelle JMoujalled Donia MSomers Klaartje - Acute myeloid leukaemia (AML) with MDS1 and EVI1 complex locus (MECOM) rearrangement is recognized by the World Health Organization as a distinct entity characterized by poor prognosis and aggressive disease progression. This rearrangement evokes aberrant ecotropic viral integration site 1 (EVI1) overexpression, which enhances leukaemic stem cell self-renewal and drives chemoresistance. However, the mechanisms by which EVI1 contributes to venetoclax resistance remain unclear. In this study, patients with AML were stratified into the EVI1-high and EVI1-low groups based on transcript levels. The EVI1-high subgroup exhibited significantly inferior clinical outcomes and reduced complete remission rates following chemotherapy or venetoclax-based regimens. Meanwhile, we demonstrated that elevated EVI1 expression confers resistance to venetoclax by stabilizing myeloid cell leukaemia 1 (MCL-1) through activation of the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT) signalling pathway in vitro. Mechanistically, elevated EVI1 levels were associated with increased phosphorylation of MCL-1 at threonine 163 (T163pMCL-1), thereby stabilizing MCL-1 by attenuating its ubiquitin-proteasome-mediated degradation. Importantly, cotreatment with venetoclax and the clinically available AKT inhibitor capivasertib effectively restored sensitivity in both cell lines and patient-derived primary AML samples with high EVI1 expression. Overall, our findings reveal a novel molecular mechanism underlying EVI1-mediated venetoclax resistance through PI3K/AKT-driven MCL-1 stabilization and suggest a combination strategy involving AKT inhibition as a promising approach for overcoming therapeutic resistance in this high-risk AML subset. - Source: PubMed
Publication date: 2026/06/04
Zhou JiayinKui XiangjieHuang DanZhang XuehongHao YuchaoXie FangLou JiachengYan Jinsong - Paediatric acute myeloid leukaemia (AML) remains a deadly disease, with survival rates reaching a plateau despite treatment with high-intensity chemotherapy. Recent advancements in therapeutic strategies, such as targeted therapies to inhibit AML dependencies, have aimed to improve outcomes. The evasion of apoptosis, regulated by the B-cell lymphoma 2 (BCL2) family of proteins, is a key feature of cancer progression and treatment resistance. Bcl-2 homology domain 3 (BH3) mimetics, such as venetoclax (ABT-199), which targets BCL2, have shown promising activity in AML. This study investigates for the first time the therapeutic potential of MIK665, a BH3 mimetic targeting myeloid cell leukaemia-1 (MCL1), in paediatric AML. We evaluated the efficacy of MIK665 against a diverse panel of AML cell lines and demonstrated its effectiveness as a single-agent treatment. Additionally, MIK665 showed significant activity against a subset of paediatric AML patient-derived xenografts (PDXs) in both ex vivo and in vivo experiments, with minimal impact on cardiac tissue pathophysiology. These findings strongly support the clinical advancement of MIK665 for paediatric AML treatment in a precision medicine approach. - Source: PubMed
Publication date: 2026/06/04
Connerty PatrickColgan John NEl-Najjar FatimaHenry EmmaXie JinhanIdais DanaGentile CarmineMao JieDolman M Emmy MMarshall Glenn MLock Richard B