Ctip1/BCL-11A Antibody (Mouse mAb) [A3G8] Datasheet

Biological Description

Specificity	Ctip1/BCL-11A Antibody (Mouse mAb) [A3G8] detects endogenous levels of total Ctip1/BCL-11A protein.
Background	CTIP1/BCL11A is a multi‑zinc‑finger transcription factor that occupies defined regulatory elements in both the β‑globin locus and the developing neocortex, where it organizes long‑range chromatin interactions and directs lineage‑specific transcriptional programs. At the human β‑globin cluster, BCL11A binds the locus control region, the ε‑globin promoter, and intergenic regions between the γ‑ and δ‑globin genes, forming a binding pattern that coincides with the fetal‑to‑adult hemoglobin switch and with a chromatin architecture in which the LCR contacts the adult β‑globin gene while interactions with γ‑globin promoters are reduced. Chromosome conformation capture and ChIP–chip data show that BCL11A participates in reconfiguring these loops and co‑occupies key sites with SOX6 and GATA1, and functional assays in adult human erythroid progenitors demonstrate that BCL11A and SOX6 cooperate to silence γ‑globin transcription, establishing BCL11A as a central component of the HbF repression complex. Genome‑wide analyses and genetic studies link erythroid BCL11A expression with HbF levels, and modulation of its dosage alters γ‑globin output in proportion to its occupancy at these regulatory elements, so BCL11A is now positioned as a primary target for HbF reactivation strategies in β‑hemoglobinopathies. In the cerebral cortex, Ctip1 is expressed by postmitotic deep‑layer projection neurons, including corticothalamic and callosal neurons, and is excluded from corticospinal motor neurons that express the related factor Ctip2, producing complementary expression domains across layer 5 and 6. Loss‑of‑function experiments show that Ctip1 is required to maintain the correct balance of deep‑layer projection neuron subtypes: deletion of Ctip1 in sensory cortex produces an excess of subcerebral projection neurons at the expense of corticothalamic and deep‑layer callosal neurons, whereas misexpression of Ctip1 represses subcerebral gene expression and their descending projections, demonstrating subtype‑specific control at the transcriptional level. Direct transcriptional targets include the cortical fate determinant Tbr1, whose repression by CTIP1 in layer 5 is necessary for acquisition of subcerebral identity, and guidance and connectivity genes such as Sema3c, which mediate neuronal polarization and radial migration of later‑born upper‑layer neurons via a defined Ctip1/Sema3c pathway. Across these systems, CTIP1/BCL11A acts through its clustered zinc fingers and corepressor‑interacting domains to bind specific promoter and enhancer sequences, assemble repressive or modulatory complexes, remodel chromatin topology, and thereby couple local transcriptional decisions to large‑scale changes in locus conformation and projection neuron wiring, linking erythroid hemoglobin switching and cortical output specification through a common transcriptional logic.

Specificity

Ctip1/BCL-11A Antibody (Mouse mAb) [A3G8] detects endogenous levels of total Ctip1/BCL-11A protein.

Background

CTIP1/BCL11A is a multi‑zinc‑finger transcription factor that occupies defined regulatory elements in both the β‑globin locus and the developing neocortex, where it organizes long‑range chromatin interactions and directs lineage‑specific transcriptional programs. At the human β‑globin cluster, BCL11A binds the locus control region, the ε‑globin promoter, and intergenic regions between the γ‑ and δ‑globin genes, forming a binding pattern that coincides with the fetal‑to‑adult hemoglobin switch and with a chromatin architecture in which the LCR contacts the adult β‑globin gene while interactions with γ‑globin promoters are reduced. Chromosome conformation capture and ChIP–chip data show that BCL11A participates in reconfiguring these loops and co‑occupies key sites with SOX6 and GATA1, and functional assays in adult human erythroid progenitors demonstrate that BCL11A and SOX6 cooperate to silence γ‑globin transcription, establishing BCL11A as a central component of the HbF repression complex. Genome‑wide analyses and genetic studies link erythroid BCL11A expression with HbF levels, and modulation of its dosage alters γ‑globin output in proportion to its occupancy at these regulatory elements, so BCL11A is now positioned as a primary target for HbF reactivation strategies in β‑hemoglobinopathies. In the cerebral cortex, Ctip1 is expressed by postmitotic deep‑layer projection neurons, including corticothalamic and callosal neurons, and is excluded from corticospinal motor neurons that express the related factor Ctip2, producing complementary expression domains across layer 5 and 6. Loss‑of‑function experiments show that Ctip1 is required to maintain the correct balance of deep‑layer projection neuron subtypes: deletion of Ctip1 in sensory cortex produces an excess of subcerebral projection neurons at the expense of corticothalamic and deep‑layer callosal neurons, whereas misexpression of Ctip1 represses subcerebral gene expression and their descending projections, demonstrating subtype‑specific control at the transcriptional level. Direct transcriptional targets include the cortical fate determinant Tbr1, whose repression by CTIP1 in layer 5 is necessary for acquisition of subcerebral identity, and guidance and connectivity genes such as Sema3c, which mediate neuronal polarization and radial migration of later‑born upper‑layer neurons via a defined Ctip1/Sema3c pathway. Across these systems, CTIP1/BCL11A acts through its clustered zinc fingers and corepressor‑interacting domains to bind specific promoter and enhancer sequences, assemble repressive or modulatory complexes, remodel chromatin topology, and thereby couple local transcriptional decisions to large‑scale changes in locus conformation and projection neuron wiring, linking erythroid hemoglobin switching and cortical output specification through a common transcriptional logic.

Usage Information

Application

WB, FCM

Dilution

WB	FCM
1:1000	1:2000

Reactivity

Mouse, Human

Source

Mouse Monoclonal Antibody

MW

91 kDa

Storage Buffer

PBS, pH 7.2+50% Glycerol+0.05% BSA+0.01% NaN3

Storage
(from the date of receipt)

-20°C (avoid freeze-thaw cycles), 2 years

References

https://pubmed.ncbi.nlm.nih.gov/27117402/
https://pubmed.ncbi.nlm.nih.gov/20395365/

Ctip1/BCL-11A Antibody (Mouse mAb) [A3G8]

Biological Description

Usage Information

References

Application Data