Dab1 polyclonal antibody
- Known as:
- Dab1 pab (anti-)
- Catalog number:
- PAB9857
- Product Quantity:
- 50 ug
- Category:
- -
- Supplier:
- Abno
- Gene target:
- Dab1 polyclonal antibody
Related genes to: Dab1 polyclonal antibody
- Gene:
- DAB1 NIH gene
- Name:
- DAB adaptor protein 1
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 1p32.2
- Locus Type:
- gene with protein product
- Date approved:
- 1998-06-12
- Date modifiied:
- 2019-01-31
Related products to: Dab1 polyclonal antibody
Related articles to: Dab1 polyclonal antibody
- The roles of Reelin and L1 cell adhesion molecule (L1CAM)-long regarded as separate regulators of neuronal migration and axon guidance-are now understood as components of a complementary signal transduction axis with significant implications for neural repair. Recent evidence has shown that Reelin activates Dab1 through the receptors ApoER2 and VLDLR, inducing Src family kinase cascades and subsequent PI3K-Akt, MAPK/ERK and cytoskeletal remodelling pathways, as well as regulating the activity of L1CAM. Particularly, Reelin seems to play a role in the neurite outgrowth promoted by L1CAM through its proteolytic cleavage, its modulation of integrin activity and the coordination of kinase binding in the axonal extension process. These meticulously synchronised processes imply that there is a common input to axonal sprouting and rearrangement of synapses as well as inflammatory regulation during the posttraumatic period of central nervous system injury. Overall, Reelin and L1CAM form a mechanistically coherent network that facilitates regeneration-related signalling, thus providing a more viable basis for new therapeutic approaches that involve the use of recombinant proteins, peptides, protease regulation or gene-directed interventions to promote neural repair. - Source: PubMed
Sahu Sudhanshu - Throughout the central nervous system, the fate and migration of projection neurons (PNs) are tightly coordinated to ensure that specific neuronal fates settle in precise spatial locations. This is particularly evident in the mammalian neocortex, where early-born PNs predominantly remain in the deeper layers of the cortical plate, whereas later-born neurons localize more superficially. However, it remains unclear whether neuronal fate acquisition directly primes the molecular mechanisms driving PN migration and positioning, or on the contrary fate and positioning are regulated independently. MicroRNAs have emerged as key regulators of cell fate determination in the neocortex. Among them, let-7 is known to influence neural progenitor competence and promote the neurogenesis of late-born PNs. Here, we show that let-7 also regulates PN migration and positioning by targeting RBX2, a core component of the E3 ubiquitin ligase CRL5, which has been previously shown to inhibit neuron migration by terminating the Reelin/DAB1 signaling pathway. Let-7 directly binds to a conserved motif in the 3'UTR of RBX2, reducing its translation and thereby diminishing CRL5 activity. Importantly, restoring RBX2 levels in the context of let-7 overexpression rescues the positioning of PNs without altering let-7-induced effects on neuronal fate. Furthermore, we demonstrate that let-7 enhances PN migration by increasing locomotion speed and prolonging migratory activity. Together, these findings reveal that let-7 coordinates neuronal fate specification and migration via distinct molecular pathways, ensuring the proper laminar positioning of late-born PNs in the neocortex. - Source: PubMed
Publication date: 2026/04/21
Decker Steven CHino KeikoLa Torre AnnaSimó Sergi - The twospot puffer (Takifugu bimaculatus) is a species of significant aquacultural value in East Asia, yet its production is constrained by slow growth rates and suboptimal body morphology. To advance genetic enhancement via marker-assisted selection, we conducted a genome-wide association study (GWAS) focusing on traits related to body shape. Utilizing a full-sib family comprising 167 individuals to reduce genetic variability, we employed whole-genome resequencing to identify 122,553 high-quality (SNPs) for association analysis. Our study identified 17 significant and suggestive SNP loci correlated with torso length (TL), body depth (BD), body width (BWI), head length (HL) and tail length (TAL). Functional annotation of surrounding genomic regions revealed 26 candidate genes associated with these traits, including lrp8, kank4 for TL; tfrc, dab1 for BD; pgm1, cp, rala, and cdh7 for BWI; gli3, sox17a, and zip12 for HL; myl9, smurf2 for TAL. These genes were implicated in skeletal development, cell migration, metabolism, and BMP/TGF-β signaling pathways. Our findings offered the first genetic insights into body shape in T. bimaculatus and provided valuable SNP markers for future genetic mapping of body shape related traits in multi-line famlies and marker-assisted selection breeding programs. - Source: PubMed
Publication date: 2026/04/01
Zhao HongbinWang LingzheChang YanwenLiang ShuangLiang JianLiu HuiruSong AnranLi LeibinGuo YongjunZhou Zhixiong - Ring finger protein 130 (RNF130) is also known as Goliath. It is the mammalian homolog of the Drosophila E3 ligase Goliath (dGoliath), which is localized to the protease-associated (PA) domain. Although RNF130 has been investigated in other research areas, its functional role in osteosarcoma remains poorly defined. - Source: PubMed
Publication date: 2026/03/31
Liu WendaGuo LiangyuLiu ZhengpingGuo Weichun - In adult superficial dorsal horn, 90% of Reelin (Reln+) and 70% of Disabled-1 (Dab1+) neurons co-express the transcription factor LIM-homeobox 1-beta (Lmx1b+) and therefore are glutamatergic neurons. Here we asked if embryonic Reln+Lmx1b+ and Dab1+Lmx1b+ dorsal horn neurons are derived from Lmx1b-expressing early-born dI5 or late-born dIL dorsal neurons. On Embryonic day (E)11.5, Reln+ and Dab1+ neurons appear to be part of the migration of early-born dI5 Lmx1b-expressing neurons. Between E12.5-E15.5, the lateral Reln+Lmx1b+ and Dab1+Lmx1b+ neurons migrate circumferentially along the rim of what will become the superficial dorsal horn, whereas medial Reln+Lmx1b+ and Dab1+Lmx1b+ neurons move into the dorsal midline and then migrate into lamina V. The small, late-born dIL Reln+Lmx1b+ and Dab1-Lmx1b+ neurons fill the superficial dorsal horn. In mutants, large Dab1+Lmx1b+ neurons were mispositioned in lamina I and at the border between the superficial and deep dorsal horn. To confirm the identity of the circumferential and midline Reln+Lmx1b+ and Dab1+Lmx1b+ neurons, we asked if they expressed the transcription factor Zfhx3, a marker of dI5 projection neurons. We detected examples of Reln+Lmx1b+Zfhx3+ and Dab1+Lmx1b+Zfhx3+ projection neurons that migrated along the outer rim of the superficial dorsal horn and others that migrated from the midline into lamina V. Taken together, our study demonstrates that the larger Reln+Lmx1b+Zfhx3+ and Dab+Lmx1b+Zfhx3+ neurons represent two subsets of dI5 projections neurons, whereas smaller Reln+Lmx1b+ and Dab1+Lmx1b+ neurons concentrated in lamina II are likely dIL interneurons. - Source: PubMed
Publication date: 2026/03/17
Yvone Griselda MChavez-Martinez Carmine LMekonnen Mahlet AZimmer SamanthaPhelps Patricia E