Human Polyclonal BAK1 Ab
- Known as:
- Human Polyclonal BAK1 Antibody
- Catalog number:
- a0204
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- ABclonal
- Gene target:
- Human Polyclonal BAK1
Related genes to: Human Polyclonal BAK1 Ab
- Gene:
- BAK1 NIH gene
- Name:
- BCL2 antagonist/killer 1
- Previous symbol:
- CDN1
- Synonyms:
- BCL2L7, BAK
- Chromosome:
- 6p21.31
- Locus Type:
- gene with protein product
- Date approved:
- 1997-10-09
- Date modifiied:
- 2016-02-24
Related products to: Human Polyclonal BAK1 Ab
Related articles to: Human Polyclonal BAK1 Ab
- Pattern-triggered immunity (PTI) is a key plant defense mechanism initiated by the recognition of pathogen-associated molecular patterns (PAMPs) by cell-surface receptors, including leucine-rich repeat receptor proteins (LRR-RPs). Upon PAMP perception, LRR-RPs associate with SOBIR1 and recruit SERK coreceptors, such as BAK1, into the receptor complex to initiate PTI. The lipase-like protein EDS1 and PAD4 are central components of effector-triggered immunity (ETI). Small molecule (SM) phosphoribosyl-AMP/ADP, generated by TIR-domain NADase activity, promotes the recruitment of helper NLRs of the ADR1 family into the EDS1-PAD4 complex to execute ETI. This ETI signaling branch, known as the EDS1-PAD4-ADR1 node, is associated with SOBIR1 and is essential for LRR-RP-mediated PTI. To elucidate the molecular mechanism by which EDS1-PAD4 contributes to PTI, we show that PTI initiation mediated by BAK1 recruitment to LRR-RP complexes is unaffected in or mutants but is abolished in the mutant, highlighting the essential role of SOBIR1 in surface immune receptor complex formation. Furthermore, we demonstrate that SM binding to EDS1 and PAD4, in addition to its role in ETI, is also critical for LRR-RP-mediated PTI, as SM-binding-deficient mutants fail to restore PTI responses. Moreover, de novo SM synthesis is required for late PTI responses, including expression and bacterial resistance, but not for early responses such as reactive oxygen species and ethylene production. Finally, the TNL SADR1 functions specifically in late PTI responses. Together, these findings indicate that a preformed EDS1-PAD4-ADR1 complex is essential for PTI and reveal a two-tiered role for TIR-domain proteins in PTI signaling. - Source: PubMed
Publication date: 2026/06/16
Fliegmann JudithJanocha DenisHua Chenleivon Roepenack-Lahaye EddaStahl MarkLocci FedericaParker Jane ENürnberger ThorstenZhang Lisha - Ustilaginoidea virens secretes numerous proteins during infection, the mechanisms regulating plant immunity and fungal virulence remain largely unknown. Herein, we identified a cortical patch protein, UvCPP1, from the U. virens secretome, as a cell death-inducing protein. UvCPP1 is secreted into rice florets via extracellular vesicles during U. virens infection. It activates plant basal immunity, as evidenced by reactive oxygen species (ROS) burst, callose deposition, and upregulation of defense-related genes. Notably, the UvCPP1 is sufficient to elicit immune responses comparable to the full-length UvCPP1. UvCPP1-induced cell death in Nicotiana benthamiana depends on brassinosteroid-insensitive 1 (BRI1)-associated receptor kinase 1 (BAK1) but is independent of suppressor of BIR1-1 (SOBIR1) and nucleotide-binding leucine-rich repeat (NLR) co-receptors. The transcript level of UvCPP1 is significantly upregulated during infection. Both knockout and overexpression of UvCPP1 significantly attenuated fungal pathogenicity, demonstrating that UvCPP1 functions as a virulence factor to promote infection and is recognized by plants. Heterologous expression of UvCPP1 significantly enhances rice immunity without compromising agronomic traits, characterized by increased ROS accumulation, callose deposition, and mitogen-activated protein kinase (MAPK) phosphorylation. UvCPP1-overexpressing lines exhibit broad-spectrum resistance against multiple pathogens. RNA-seq analysis revealed that UvCPP1 expression activates defense-related genes, phytohormone signaling pathways, and diterpenoid biosynthesis. Although UvCPP1 is indispensable for the full virulence of U. virens, it simultaneously activates plant immune responses. The characteristics of UvCPP1 highlight its potential application as a molecular tool for breeding disease-resistant crops through immune priming, offering a sustainable strategy for false smut management. - Source: PubMed
Wang XiuXiong JinliSun YuchenFang YuanLi WenjingGuo WeiChen XiaoyangWang ZhaoyunPan Yuemin - Plant morphology is a critical determinant of crop productivity in Brassica napus, influencing both lodging resistance and optimal planting density. Here, we investigated the genetic regulation of plant architecture by focusing on the BAK gene family. Using a multi-target sgRNA CRISPR/Cas9 strategy, we generated knockout mutants of several BAK homologs. Phenotypic characterization showed that specific higher-order mutants (Bnbak_sp and Bnbak_n) displayed significantly reduced plant height and altered silique arrangement, while maintaining normal yield-related traits. Expression and localization analyses revealed that BnBAK genes are primarily expressed in leaves and stem internodes, with proteins localizing to multiple membrane systems, including the nuclear envelope. Transcriptomic analysis of internodes indicated extensive reprogramming of photosynthesis- and defense-related pathways. Additionally, we identified TCP transcription factors as key downstream regulators, with motif enrichment confirming TCP-binding sites in promoters of differentially expressed genes. Furthermore, BnBAK proteins are required for the accumulation of BnTCP transcription factors in planta. Functional complementation in Arabidopsis further demonstrated that overexpression of TCP21 substantially rescued the dwarf phenotype of bak1-3 bkk1-1 mutants. Together, these findings elucidate the molecular mechanisms through which BnBAK genes modulate plant architecture in B. napus, providing critical insights and practical targets for breeding compact, high-yielding rapeseed varieties. - Source: PubMed
Publication date: 2026/06/14
Zhang YuanbinGuo YiyiSun RuiLou XinyiCai ShengguanDong JieWang RuiBai Yuxue - Given the known therapeutic properties of gold compounds such as auranofin, this study aimed to evaluate the anticancer potential of a newly synthesized gold(III) Schiff base complex. We hypothesized that this complex could selectively induce apoptosis in cancer cells while minimizing inflammatory responses in normal cells. - Source: PubMed
Publication date: 2026/06/09
Lu XiaolongMajd Mostafa HeidariShahraki SomayeLi Shang - Vasculogenic mimicry (VM) refers to the capacity of cancer cells from aggressive tumors to form a set of sinuses and channels that mimic normal blood vessels and lack endothelial cells. The rapid growth of a tumor leads to a deficiency in normal vessels, followed by poor oxygen and nutrient supply to tumor cells and VM induction. Understanding the mechanisms behind the development of the VM phenotype is important for the development of new anti-cancer therapies. Previous reports indicate that, during VM formation by melanoma Mel Z cells, about 2000 developmental genes undergo dramatic changes in expression. To identify genes more tightly linked to VM development, we compared the transcriptomes of Mel Z and MDA-MB-231 cells (triple-negative breast cancer cells), which also form VM. Most of the genes that change expression differ substantially between these two cell types. However, we identified 51 up- and 98 downregulated genes common to both cell lines. The non-overlapping groups of these genes are involved in regulating cell adhesion and proliferation. The group of common upregulated genes includes nine genes controlling blood vessel development and tube morphogenesis. Two genes in this group ( and ) rapidly form numerous contacts with nucleoli during VM phenotype formation. We observed that knockdown of the gene prevents the development of VM in Mel Z cells. Our data indicate that the formation of VM by aggressive cancer cells might be controlled by a special set of genes. - Source: PubMed
Publication date: 2026/05/29
Tchurikov Nickolai AKlushevskaya Elena SLukicheva Viktoriya NKretova Antonina NChechetkin Vladimir RKravatskaya Galina IVartanian Amalia AAlembekov Ildar RKravatsky Yuri V